Veröffentlicht am 25.05.2012
https://www.iarc.fr/en/media-centre/pr/2012/pdfs/pr213_E.pdfPRESS RELEASE N° 213
>>>> 12 June 2012IARC:
DIESEL ENGINE EXHAUST CARCINOGENICLyon, France, June 12, 2012 ‐‐ After a week-long meeting of international experts, the International
Agency for Research on Cancer (IARC), which is part of the World Health Organization (WHO), today
classified diesel engine exhaust as carcinogenic to humans (Group 1), based on sufficient evidence
that exposure is associated with an increased risk for lung cancer.
Background
In 1988, IARC classified diesel exhaust as probably carcinogenic to humans (Group 2A). An Advisory Group
which reviews and recommends future priorities for the IARC Monographs Program had recommended
diesel exhaust as a high priority for re-evaluation since 1998.
There has been mounting concern about the cancer-causing potential of diesel exhaust, particularly based
on findings in epidemiological studies of workers exposed in various settings. This was re-emphasized by
the publication in March 2012 of the results of a large US National Cancer Institute/National Institute for
Occupational Safety and Health study of occupational exposure to such emissions in underground miners,
which showed an increased risk of death from lung cancer in exposed workers (1).
EvaluationThe scientific evidence was reviewed thoroughly by the Working Group and overall it was concluded that there was sufficient evidence in humans for the carcinogenicity of diesel exhaust. The Working Group found that diesel exhaust is a cause of lung cancer (sufficient evidence) and also noted a positive association (limited evidence) with an increased risk of bladder cancer (Group 1). BENZINE-uitlaatgassen incl -roet >>>: The Working Group concluded that gasoline exhaust was possibly carcinogenic to humans (Group 2B), a finding unchanged from the previous evaluation in 1989.Public health
Large populations are exposed to diesel exhaust in everyday life, whether through their occupation or
through the ambient air. People are exposed not only to motor vehicle exhausts but also to exhausts from
other diesel engines, including from other modes of transport (e.g. diesel trains and ships) and from power
generators.
Given the Working Group’s rigorous, independent assessment of the science, governments and other
decision-makers have a valuable evidence-base on which to consider environmental standards for diesel
exhaust emissions and to continue to work with the engine and fuel manufacturers towards those goals.
Increasing environmental concerns over the past two decades have resulted in regulatory action in North
America, Europe and elsewhere with successively tighter emission standards for both diesel and gasoline
engines. There is a strong interplay between standards and technology – standards drive technology and
new technology enables more stringent standards. For diesel engines, this required changes in the fuel
such as marked decreases in sulfur content, changes in engine design to burn diesel fuel more efficiently
and reductions in emissions through exhaust control technology.
However, while the amount of particulates and chemicals are reduced with these changes, it is not yet
clear how the quantitative and qualitative changes may translate into altered health effects; research into
this question is needed. In addition, existing fuels and vehicles without these modifications will take many
years to be replaced, particularly in less developed countries, where regulatory measures are currently
also less stringent. It is notable that many parts of the developing world lack regulatory standards, and
data on the occurrence and impact of diesel exhaust are limited.
Conclusions
Dr Christopher Portier, Chairman of the IARC working Group, stated that “The scientific evidence was
compelling and the Working Group’s conclusion was unanimous: diesel engine exhaust causes lung
cancer in humans.” Dr Portier continued: “Given the additional health impacts from diesel particulates,
exposure to this mixture of chemicals should be reduced worldwide.“(2)
Dr Kurt Straif, Head of the IARC Monographs Program, indicated that “The main studies that led to this
conclusion were in highly exposed workers. However, we have learned from other carcinogens, such as
radon, that initial studies showing a risk in heavily exposed occupational groups were followed by positive
findings for the general population. Therefore actions to reduce exposures should encompass workers
and the general population.”
Dr Christopher Wild, Director, IARC, said that “while IARC’s remit is to establish the evidence-base for
regulatory decisions at national and international level, today’s conclusion sends a strong signal that
public health action is warranted. This emphasis is needed globally, including among the more vulnerable
populations in developing countries where new technology and protective measures may otherwise take
many years to be adopted.”
Summary evaluation
The summary of the evaluation will appear in The Lancet Oncology as an online publication ahead of print on June 15, 2012.
(1) JNCI J Natl Cancer Inst (2012) doi:10.1093/jnci/djs034
http://jnci.oxfordjournals.org/content/early/2012/03/05/jnci.djs034.abstract; and
JNCI J Natl Cancer Inst (2012) doi: 10.1093/jnci/djs035
http://jnci.oxfordjournals.org/content/early/2012/03/05/jnci.djs035.abstract(2) Dr Portier is Director of the National Center for Environmental Health and the Agency for Toxic
Substances and Disease Registry at the Centers for Disease Control and Prevention (USA).
page 3
Evaluation groups - DefinitionsGroup 1: The agent is carcinogenic to humans.
This category is used when there is sufficient evidence of carcinogenicity in humans. Exceptionally, an
agent may be placed in this category when evidence of carcinogenicity in humans is less than sufficient
but there is sufficient evidence of carcinogenicity in experimental animals and strong evidence in exposed
humans that the agent acts through a relevant mechanism of carcinogenicity.Group 2.
This category includes agents for which, at one extreme, the degree of evidence of carcinogenicity in
humans is almost sufficient, as well as those for which, at the other extreme, there are no human data but
for which there is evidence of carcinogenicity in experimental animals. Agents are assigned to either
Group 2A (probably carcinogenic to humans) or Group 2B (possibly carcinogenic to humans) on the basis
of epidemiological and experimental evidence of carcinogenicity and mechanistic and other relevant data.
The terms probably carcinogenic and possibly carcinogenic have no quantitative significance and are
used simply as descriptors of different levels of evidence of human carcinogenicity, with probably
carcinogenic signifying a higher level of evidence than possibly carcinogenic.
Group 2A: The agent is probably carcinogenic to humans.
This category is used when there is limited evidence of carcinogenicity in humans and sufficient
evidence of carcinogenicity in experimental animals. In some cases, an agent may be classified in
this category when there is inadequate evidence of carcinogenicity in humans and sufficient
evidence of carcinogenicity in experimental animals and strong evidence that the carcinogenesis
is mediated by a mechanism that also operates in humans. Exceptionally, an agent may be
classified in this category solely on the basis of limited evidence of carcinogenicity in humans. An
agent may be assigned to this category if it clearly belongs, based on mechanistic considerations,
to a class of agents for which one or more members have been classified in Group 1 or Group 2A.
>>> BENZINE-uitlaatgassen: Group 2B: The agent is possibly carcinogenic to humans.
This category is used for agents for which there is limited evidence of carcinogenicity in humans
and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used
when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of
carcinogenicity in experimental animals. In some instances, an agent for which there is
inadequate evidence of carcinogenicity in humans and less than sufficient evidence of
carcinogenicity in experimental animals together with supporting evidence from mechanistic and
other relevant data may be placed in this group. An agent may be classified in this category solely
on the basis of strong evidence from mechanistic and other relevant data.Group 3: The agent is
not classifiable as to its carcinogenicity to humans.
This category is used most commonly for agents for which the evidence of carcinogenicity is
inadequate in
humans and inadequate or limited in experimental animals. ...]
~ idem Nederlandstalige uitleg van hierboven:
http://www.vmx.be/who-diesel-kankerverwekkend ook:
http://www.ademloos.be/nieuws/we-hebben-de-meest-kankerverwekkende-wagenvloot-europa OESO/andere
We hebben de meest kankerverwekkende wagenvloot in Europa
21/09/13
In deze Vrije Tribune gaat Dr. Christophe Depamelaere op zoek naar het verband tussen de hoge kankerscores in ons land en het politieke beleid dat dieselverkeer aanmoedigt.
‘Avoiding death by diesel’ door Simon Upton, hoofd Milieu Oeso, inspireert:
De schadelijke uitstoot door verkeer, veroorzaakt zowat tien keer meer doden dan verkeersongevallen. De vermindering van de levensverwachting bedraagt in een stad als Antwerpen zowat drie jaar. Terecht maant de WHO politici aan de bevolking beter tegen luchtpollutie te beschermen, omdat dit ver buiten de controle van het individu ligt. Een uitgebreide Europese studie (Escape) wijst op het lineaire verband tussen (diesel)fijnstof en longadenocarcinoom. In de nabeschouwing wijst men er wel op dat fijnstof, net zoals roken, een controleerbare factor is. In België, met zijn uitgebreide vloot bedrijfswagens, kan het probleem inderdaad fiscaal snel worden bijgestuurd...
Het politieke beleid gevoerd in België staat helaas haaks op deze aanmanende studies. Dieselverkeer, de hoofdbron van fijnstof, wordt via gedwongen dieselbedrijfswagens (97,5%) en een bloeiende tweedehandsmarkt (62,4%) steeds talrijker. Bovendien wordt de dieselvloot steeds ouder, met nog meer fijnstof tot gevolg. De petroleumfederatie meldt aldus een onzinnige verkoop van 84% dieselbrandstof in dichtbevolkt België.
Het lijkt wel alsof de federale overheid eerder aanstuurt op gezondheidsschade, dan wel op bescherming. Vooral minister Onkelinx draagt mede grote schuld door bedrijven sinds 2012 quasi volledig richting diesel te duwen, door CO2 en prijsgebonden VAA (Voordeel Alle Aard), fiscale aftrek en pervers dure benzine (36% hogere accijnzen dan voor diesel aan de pomp). Benzine, goedkoper op de internationale markt, wordt ‘fiscaal’ duur aan de pomp. Hierdoor dient Vlaanderen jaarlijks 5,22 miljard aan ‘medische dieselzorg’ te spenderen.
‘Avoid cancer by diesel’, Christophe Depamelaere: Onkelinx en co voorzagen dichtbevolkt België aldus van de meest kankerverwekkende wagenvloot in Europa. De bereikte resultaten gepubliceerd in Health at a glance Europe 2012 spreken alvast boekdelen: een absolute topscore voor borstkanker-incidentie (53% boven EU gemiddelde), alsook hoogste mortaliteit. Dit wijst vermoedelijk op veel te laat ontdekte agressieve tumoren, ondanks onze screeningprogramma’s. Wij kennen de derde positie voor prostaatkanker (60% boven EU gemiddelde) en vierde positie voor longkanker (21% boven EU gemiddelde), met ook in deze twee gevallen de hoogste mortaliteit in Europa.
Dieselwerend USA kent 30% minder borstkanker. Dieselwerend Japan 50% minder borst- en 66% minder prostaatkanker (IARC/Globocan). Gezien de Belgen Europa’s grootste fruit- en groenteneters in Europa zijn, lijkt onze voeding alvast niet de hoofdreden te zijn. Een benzinekatalysator kan tot 90% PAKs (polycyclische aromatische koolwaterstoffen) neutraliseren, een dieselkatalysator kan dat niet. Diesel staat in voor 96,8% van de NO2(stikstofdioxides), gevormd voor 63% door het verkeer. Bovendien zorgen ze vooral voor een toename van de totale genotoxische activiteit van de PAKs, door vorming van nitro-PAKs. Het volume PAKs door (diesel)verkeer is sinds 2000 met 50% gestegen, een bewijs temeer dat de totale mutagene activiteit van ons verkeer zwaar onderschat wordt!
De WGO erkent in haar Revihaap review dat het totale carcinogeen vermogen van de PAKs, met BaP benzo(a)pyreen (een gemiddeld potent carcinogeen) als enige indicator, vermoedelijk wordt onderschat. Toch hanteert zij een veiligheidslimiet die 100x boven de Amerikaanse (Epa) ligt. Zij wijst ook op het grote verschil tussen benzineversus dieselkatalysator, maar ontraadt diesel vervolgens niet. De Oeso doet dat wel en wijst zelfs op de te mijden hefboom die diesel op de vergrijzingskost vormt.
Kleine benzinemotoren stelt zij voorop als remedie. Ook pleit de Oeso voor hogere dieseltaks. Zelf pleit ik voor lagere benzinetaks als promoverende game-changer voor onze economische competitiviteit en gezondheid!
‘Avoid drugs and stents by diesel’...
Dieselroet veroorzaakt plaques, vasoconstrictie, trombogeniciteit en verhoogt hierdoor onze doodsoorzaak nummer één: hart- en vaatziek-
ten. Gevolg is een twee tot drie keer hoger cardovasculair risicoprofiel, dat ons dwingt tot het gebruik van meer bloeddruk- of cholesterolverlagers en zelfs coronaire stents, tot ruim het dubbele van het Europees gemiddelde. Diesel zorgt ook voor meer fertiliteitsproblematiek, meer prematuren, meer IUGR, meer COPD, type 1 diabetes en astma bij kinderen... Besparingen Onkelinx?
Dr. Christophe Depamelaere, huisarts/sportarts, Wingene ARTSENKRANT 20-09-2013
En hoe fijner de dieselroetdeeltjes hoe giftiger, moderne dieselmotoren zijn dus eigenlijk niet onschadelijker als oudere diesels betreft roetdeeltjes...
Dit is ook wetenschappelijk aangetoond:
http://pubs.acs.org/doi/full/10.1021/es4003873 nog eens in 2013
(er is ook een studie van 2008 (Max Planck Institut, die ik al jaren geleden geciteerd heb)
Diesel Soot Toxification
Benjamin Frank†, Robert Schlögl†, and Dang Sheng Su*†‡
† Department of Inorganic Chemistry, Fritz Haber Institute of the Max Planck Society, Berlin 14195, Germany
‡ Shenyang National Laboratory for Materials Science, Institute of Metal Research, Chinese Academy of Science, Shenyang 110016, China
Environ. Sci. Technol., 2013, 47 (7), pp 3026–3027
DOI: 10.1021/es4003873
Publication Date (Web): March 11, 2013
Copyright © 2013 American Chemical Society
Economic and environmental amenities of diesel engines such as high fuel efficiency led to a steady increase in popularity.(1) However, their major disadvantage with regard to environmental and health protection is the typically enhanced production of diesel particulate matter (DPM) comprising soot and unburned carbonaceous compounds. Stricter emission levels, for example, the Euro I to VI standards in the European Union, and tax incentives are imposed. One strategy to lower this burden is the optimization of fuel combustion in the engine as typically realized by a turbocharger. Here, the drastically lowered fuel droplet size negatively influences the DPM nanostructure. Smaller particles may penetrate more deeply into the respiratory tract, where their large surface-to-volume ratio could allow for more biological interaction. It could turn out to be ironical history that huge effort made in this direction is driven by the increasing awareness of the public on the toxicity of diesel.
What are the structural and chemical features of low-emission DPM on the nanoscale? The most evident change is in the size of primary soot particles as evidenced for common heavy-duty diesel engines fulfilling the Euro III, IV, and VI standard. Here, the average diameter steadily decreased from 30–40 nm down to 10–15 nm.(2) The second significant trend is the more defective bulk and surface structure as the result of alteration of the fuel combustion process. The enhanced localization of conjugated π-electrons on graphitic surfaces generates favored anchoring points for surface functional groups by reaction with water or oxygen. The consequence is an abundance of chemically reactive oxygen functional groups on the highly defective modern low-emission diesel soot.
The chemical activation of the DPM is astonishing. The carbon surface in its initial highly functionalized state shows an outstanding activity in heterogeneous catalysis. The oxidative dehydrogenation of ethylbenzene to styrene and the selective oxidation of acrolein to acrylic acid are large-scale chemical processes and are catalyzed by highly developed promoted (mixed) oxides with excess of steam, respectively. However, they were also proven to be successfully catalyzed by nanostructured carbon materials. We were surprised to see that the initial productivity of the untreated soot of a Euro IV test engine used as the catalyst in these reactions exceeds the data of well performing other carbonaceous materials.(1) Especially the curvature of the outermost carbon shells (Figure 1), which is more pronounced the smaller the spherical carbon particles are, promotes the activation of molecular oxygen.
DPM as a major constituent of air pollution is associated with respiratory and cardiovascular diseases as well as skin cell alterations. Like airway epithelial cells, the epidermal cells are among the first cell populations exposed to chemical pollutants and are an important source of pro-inflammatory mediators. Soot nanoparticles are spontaneously internalized by keratinocytes and distributed mostly around the cell nucleus.(3) Low-emission Euro IV soot particles exhibit a very high oxidative, pro-fibrotic, and toxic potential on these cell types. Further irrefutable environmental consequences and health effects are seen in an increased cytotoxicity and inflammatory potential of Euro IV soot toward human peripheral blood monocyted-derived macrophage cells (MDM). Euro IV soot exhibits a much higher toxic and inflammatory potential than Euro III particles.(2) The latter did not induce any significant signs of necrosis or apoptosis, whereas Euro IV DPM produces extensive damage of the cells.
In addition to these alarming effects of as-produced DPM a fatal postactivation can proceed. The heterogeneous reactions of aerosol particles with ozone, which is ubiquitously formed in traffic zones by UV radiation induced reactions of nitric oxide with molecular oxygen, are of central importance to air quality.(4) Reactive oxygen intermediates with a lifetime greater than 100 s can play a key role in the chemical transformations and adverse health effects of toxic and allergenic air-particulate matter, such as soot, polycyclic aromatic hydrocarbons, and proteins.
Thus, the major question arises whether the emissions of modern diesel engines are characterized by a potentially greater threat to human beings. The answer is not straightforward. The reduction of the emission rate of soot nanoparticulate does not automatically lead to a reduction of the toxic effects toward humans if, concurrently, the structure and functionality of the soot changes and therefore its biological, cytotoxic and inflammatory potential, increase. Clearly, on the qualitative basis, the low-emission soot imposes higher risks. On the other hand, its total amount is substantially lower than for the older generations of diesel engines. Within the past 20 years the DPM emission level for diesel engines was decreased by almost 2 orders of magnitude rendering an evaluation, which combines qualitative and quantitative aspects, difficult. Although the development of improved particle filters and novel methods for particulate removal in diesel cars is an ongoing task for industry the ultimate answer could be given by the future statistical analysis of mortality due to soot exposition. For 2003 in Germany, 10 000–19 000 diesel soot-related deaths, for example, due to lung cancer, were estimated as a result of long-term effects.(5) The future course of this death rate will be the final benchmark for the appraisal of past and current efforts to overcome the environmental and health burden of the diesel engine technology.
The authors declare no competing financial interest.
Soit, menig land denkt al een stap verder en gaat electrische alternatieven promoten, zelfs Oostenrijk (die tot hun spijt ook veel diesels hebben):
http://autorevue.at/autowelt/oesterreich-2020-diesel-bezinautos
UMWELTBUNDESAMT: AUCH IN ÖSTERREICH SOLLTEN AB 2020 KEINE DIESEL- UND BENZINAUTOS MEHR VERKAUFT WERDEN
Das Umweltbundesamt fordert, den Verkauf von „konventionellen Pkw“ ab 2020 „stark einzuschränken“ und nur mehr Elektroautos zu verkaufen – „bestehende Fahrzeuge greifen wir nicht an“
13.04.2016
Noorwegen plant zelfs het verbieden vanaf 2025, zelfs bij bestelwagens:
http://autorevue.at/autowelt/norwegen-verbietet-benzin-dieselautos
NORWEGEN WILL BENZIN- UND DIESELAUTOS AB 2025 VERBIETEN
Bereits ab 2025 sollen in Norwegen nur mehr Elektroautos zugelassen werden – auch Nutzfahrzeuge sind betroffen.
24.03.2016 Tamara Schögl APA
Norwegen will als erstes Land der Welt Benzin- und Dieselautos verbieten. Bereits ab 2025 sollen nur mehr Elektroautos verkauft werden dürfen. Gleichzeitig sollen Radwege und Öffis massiv ausgebaut werden. Das sieht der vor wenigen Tagen vorgestellte „National Transit Plan“ für die Jahre 2018 bis 2029 laut Medienberichten vor. Das Parlament muss dem Vorhaben erst zustimmen.
AUCH NUTZFAHRZEUGE BETROFFEN
Natuurlijk vooral landen met véél groene stroom(mogelijkheden).