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  1. Air Quality Guidelines for Europe 2nd edition (WHO Regional Publications. European Series)
  2. Navigointivalikko
  3. Exceedance of air quality standards in urban areas
  4. Indicator specification and metadata
  5. E-PACK Europe E-commerce & Packaging Industry Conference

Agents, mixtures and exposure circumstances 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 other relevant data. Group 2A the agent mixture is probably carcinogenic to humans. The exposure circumstance entails exposures that are 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 mixture 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, mixture or exposure circumstance may be classified in this category solely on the basis of limited evidence of carcinogenicity in humans.

Group 2B the agent mixture is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances 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, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.

This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals.

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Air Quality Guidelines for Europe 2nd edition (WHO Regional Publications. European Series)

Exceptionally, agents mixtures for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category. Group 4 The agent mixture is probably not carcinogenic to humans. This category is used for agents or mixtures for which there is evidence suggesting lack of carcinogenicity in humans and in experimental animals.

In some instances, agents or mixtures for which there is inadequate evidence of carcinogenicity in humans but evidence suggesting lack of carcinogenicity in experimental animals, consistently and strongly supported by a broad range of other relevant data, may be classified in this group. Source: IARC The choice of the extrapolation model depends on the current understanding of the mechanisms of carcinogenesis 13 , and no single mathematical procedure can be regarded as fully appropriate for low-dose extrapolation.

Methods based on a linear, non-threshold assumption have been used at the national and international level more frequently than models that assume a safe or virtually safe threshold. In these guidelines, the risk associated with lifetime exposure to a certain concentration of a carcinogen in the air has been estimated by linear extrapolation and the carcinogenic potency expressed as the incremental unit risk estimate. By using unit risk estimates, any reference to the acceptability of risk is avoided.

The decision on the acceptability of a risk should be made by national authorities within the framework of risk management. To support authorities in the decision-making process, the guideline sections for carcinogenic pollutants provide the concentrations in air associated with an excess cancer risk of 1 in a population of , 1 in or 1 in , respectively, calculated from the unit risk. For those substances for which appropriate human studies are available, the method known as the average relative risk model has been used, and is therefore described in more detail below.

Several methods have been used to estimate the incremental risks based on data from animal studies. Two general approaches have been proposed. Nonlinear relations have been proposed for use when the data derived from animal studies indicate a nonlinear dose response relationship or when there is evidence that the capacity to metabolize the polluting chemical to a carcinogenic form is of limited capacity. Quantitative assessment of carcinogenicity based on human data Quantitative assessment using the average relative risk model comprises four steps: a selection of studies; b standardized description of study results in terms of relative risk, exposure level and duration of exposure; c extrapolation towards zero dose; and d application to a general hypothetical population.

First, a reliable human study must be identified, where the exposure of the study population can be estimated with acceptable confidence and the excess cancer incidence is statistically significant. If several studies exist, the best representative study should be selected or several risk estimates evaluated. Once a study is identified, the relative risk as a measure of response is calculated. It should be noted that the unit lifetime risk depends on P 0 background lifetime risk , which is determined from national age-specific cancer incidence or mortality rates.

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Since these rates are also determined by exposures other than the one of interest and may vary from country to country, it follows that the UR may also vary from one country to another. Necessary assumptions for average relative risk method Before any attempt is made to assess the risk in the general population, numerous assumptions are needed at each phase of the risk assessment process to fill in various gaps in the underlying scientific database. As a first step in any given risk assessment, therefore, an attempt should be made to identify the major assumptions that have to be made, indicating their probable consequences.

These assumptions are as follows. The response measured as relative risk is some function of cumulative dose or exposure.

There is no threshold dose for carcinogens. Many stages in the basic mechanism of carcinogenesis are not yet known or are only partly understood.


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Taking available scientific findings into consideration,. This view is based on the fact that most agents that cause cancer also cause irreversible damage to deoxyribonucleic acid DNA. The assumption applies for all non-threshold models. The linear extrapolation of the dose response curve towards zero gives an upper-bound conservative estimate of the true risk function if the unknown true dose response curve has a sigmoidal shape.

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The scientific justification for the use of a linear non-threshold extrapolation model stems from several sources: the similarity between carcinogenesis and mutagenesis as processes that both have DNA as target molecules; the strong evidence of the linearity of dose response relationships for mutagenesis; the evidence for the linearity of the DNA binding of chemical carcinogens in the liver and skin; the evidence for the linearity in the dose response relationship in the initiation stage of the mouse 2-stage tumorigenesis model; and the rough consistency with the linearity of the dose response relationships for several epidemiological studies.

This assumption applies for all linear models. There is constancy of the relative risk in the specific study situation. The advantage of the average relative risk method is that this needs to be true only for the average. Advantages of the method The average relative risk method was selected in preference to many other more sophisticated extrapolation models because it has several advantages, the main one being that it seems to be appropriate for a fairly large class of different carcinogens, as well as for different human studies.

This is possible because averaging doses, that is, averaging done over concentration and duration of exposure, gives a reasonable measure of exposure when dose rates are not constant in time. This may be illustrated by the fact that the use of more sophisticated models 14, 18, 19 results in risk estimates very similar to those obtained by the average relative risk method. Another advantage of the method is that the carcinogenic potency can be calculated when estimates of the average level and duration of exposure are the only known parameters besides the relative risk.

Furthermore, the method has the advantage of being simple to apply, allowing non-experts in the field of risk models to calculate a lifetime risk from exposure to the carcinogens. There are specific situations, however, in which the method cannot be recommended, mainly because the assumptions do not hold true. The cumulative dose concept, for instance, is inappropriate when the mechanism of the carcinogen suggests that it cannot produce cancer throughout all stages of the cancer development process.

Also, specific toxicokinetic properties, such as a higher excretion rate of a carcinogen at higher doses or a relatively lower production rate of carcinogenic metabolites at lower doses, may diminish the usefulness of the method in estimating cancer risk. Furthermore, supralinearity of the dose response curve or irregular variations in the relative risk over time that cannot be eliminated would reduce the value of the model. Nevertheless, evidence concerning these limitations either does not exist or is still too preliminary to make the average relative risk method inappropriate for carcinogens evaluated here.

A factor of uncertainty, rather than of methodological limitation, is that data on past exposure are nearly always incomplete. Although it is generally assumed that in the majority of studies the historical dose rate can be determined within an order of magnitude, there are possibly greater uncertainties, even of more than two orders of magnitude, in some studies. In the risk assessment process it is of crucial importance that this degree of uncertainty be clearly stated. This is often done simply by citing upper and lower limits of risk estimates.

Exceedance of air quality standards in urban areas

Duration of exposure and the age- and time-dependence of cancer caused by a particular substance are less uncertain parameters, although the mechanisms of relationship are not so well understood Risk estimates from animal cancer bioassays Animal bioassays of chemicals provide important information on the human risk of cancer from exposure to chemicals. These data enhance our confidence in assessing human cancer risks on the basis of epidemiological data.

There is little doubt of the importance of animal bioassay data in reaching an informed decision on the carcinogenic potential of a chemical. The collection and use of data such as those on saturation mechanisms, absorption, distribution and metabolic pathways, as well as on interaction with other chemicals, is important and should be continued.

Regrettably, these data were not always available for the air pollutants evaluated during the update and revision of the guidelines. The process of evaluating guidelines. Several chemicals considered in this publication have been studied using animal cancer bioassays. The process is continuing and new information on the potential carcinogenicity of chemicals is rapidly appearing. Consequently, the status of chemicals is constantly being reassessed. There is no clear consensus on appropriate methodology for the risk assessment of chemicals for which the critical effect may not have a threshold, such as genotoxic carcinogens and germ cell mutagens.

A number of approaches based largely on characterization of dose response have been adopted for assessment of such effects: quantitative extrapolation by mathematical modelling of the dose response curve to estimate the risk at likely human intakes or exposures low-dose risk extrapolation ; relative ranking of potencies in the experimental range; and division of effect levels by an uncertainty factor.

Low-dose risk extrapolation has been accomplished by the use of mathematical models such as the Armitage-Doll multi-stage model.


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In more recently developed biological models, the different stages in the process of carcinogenesis have been incorporated and time to tumour has been taken into account In some cases, such as that of butadiene, uncertainty regarding the metabolism in humans and experimental animals precluded the choice of the appropriate animal model for low-dose risk extrapolation. In other cases where data permitted, attempts were made to incorporate the dose delivered to the target tissue into the dose response analysis physiologically based pharmacokinetic modelling.

During revision of the guidelines, other approaches to establishing guideline levels for carcinogens were considered. Such approaches involve the identification of a level of exposure at which the risk is known to be small and the application of uncertainty factors to derive a level of exposure at which the risk is accepted as being exceedingly small or negligible. This approach has been adopted in the United Kingdom, for example. It was agreed that such an approach might be applicable on a national or smaller scale, but that it was unlikely to be generally applicable.

Interpretation of risk estimates The risk estimates presented in this book should not be regarded as being equivalent to the true cancer risk.

Indicator specification and metadata

It should be noted that crude expression. Estimated risks are believed to represent only the plausible upper bounds, and may vary widely depending on the assumptions on which they are based. The presented quantitative risk estimates can provide policy-makers with rough estimates of risk that may serve well as a basis for setting priorities, balancing risks and benefits, and establishing the degree of urgency of public health problems among subpopulations inadvertently exposed to carcinogens. A risk management approach for compounds for which the critical effect is considered not to have a threshold involves eliminating or reducing exposure as far as practically or technologically possible.

Characterization of the dose response, as indicated in the procedures described above, can be used in conjunction with this approach to assess the need to reduce exposure. Combined exposures Exposure to combinations of air pollutants is inevitable. Data dealing with the effects of co-exposure to air pollutants are, however, very limited and it is not possible to recommend guidelines for such combinations.

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Of course, measures taken to control air pollution frequently lead to the reduction in concentrations of more than one pollutant. This is often achieved by controlling sources of pollutants rather than by focusing on individual pollutants. Ecological effects may have a significant indirect influence on human health and wellbeing. For example, most of the major urban air pollutants are known to have adverse effects at low levels on plants, including food crops.

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A consultation group was therefore convened to consider the ecological effects on terrestrial vegetation of sulfur dioxide, nitrogen dioxide, and ozone and other photochemical oxidants. These substances are important both because of the high anthropogenic amounts produced and because of their wide distribution. They deserve special attention because of significant adverse effects on ecological systems in concentrations far below those known to be harmful to humans. The pollutants selected for consideration here form only part of the vast range of air pollutants that have ecological effects.