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Objectives-To evaluate the eYciency of diVerent automotive cabin air filters to prevent penetration of components of diesel exhaust and thereby reduce biomedical eVects in human subjects. Filtered air and unfiltered diluted diesel exhaust (DDE) were used as negative and positive controls, respectively, and were compared with exposure to DDE filtered with four diVerent filter systems. Methods-32 Healthy non-smoking subjects (age 21-53) participated in the study. Each subject was exposed six times for 1 hour in a specially designed exposure chamber: once to air, once to unfiltered DDE, and once to DDE filtered with the four diVerent cabin air filters. Particle concentrations during exposure to unfiltered DDE were kept at 300 µg/m 3 . Two of the filters were particle filters. The other two were particle filters combined with active charcoal filters that might reduce certain gaseous components. Subjective symptoms were recorded and nasal airway lavage (NAL), acoustic rhinometry, and lung function measurements were performed. Results-The two particle filters decreased the concentrations of diesel exhaust particles by about half, but did not reduce the intensity of symptoms induced by exhaust. The combination of active charcoal filters and a particle filter significantly reduced the symptoms and discomfort caused by the diesel exhaust. The most noticable diVerences in eYcacy between the filters were found in the reduction of detection of an unpleasant smell from the diesel exhaust. In this respect even the two charcoal filter combinations diVered significantly. The eYcacy to reduce symptoms may depend on the abilities of the filters investigated to reduce certain hydrocarbons. No acute eVects on NAL, rhinometry, and lung function variables were found. Conclusions-This study has shown that the use of active charcoal filters, and a particle filter, clearly reduced the intensity of symptoms induced by diesel exhaust. Complementary studies on vehicle cabin air filters may result in further diminishing the biomedical eVects of diesel exhaust in subjects exposed in traYc and workplaces. (Occup Environ Med 1999;56:222-231)

SummaryThe Institute of Environmental Medicine (IMM) in Stockholm has recommended health-based guideline values (low-risk levels) for a number of carcinogenic air pollutants. In these risk assessments, mathematical extrapolation models have only been used for some genotoxic compounds or compounds giving rise to genotoxic metabolites. For other carcinogenic compounds a NOEL, LOEL/uncertainty factor approach has been used. In this paper the IMM risk assessments are commented upon, and comparisons are made with the corresponding risk assessments from US EPA and WHO.This report was originally presented at a seminar in December 1987 entitled "Carcinogen Risk Assessment: models and their applications". The seminar was arranged by the Swedish Toxicological Council and the proceedings will appear as a report from the National Chemicals Inspectorate. 4 IntroductionAt the Institute of Environmental Medicine (IMM), we have performed quantitative risk assessments of carcinogens at several occacions, mainly at the request of the Swedish Environmental Protection Agency to propose health based environmental guideline values for ambient air. In these cases the quantitative risk assessment is the final part of a larger effort that consists of collecting, reading, summarizing and evaluating the available literature. Some large epidemiological studies performed at the IMM have also led to quantitative risk estimates, such as one concerning the risk of lung cancer due to radon in homes. In this paper the basis for the risk assessment of some air pollutants will be discussed.When evaluating compounds for which there are epidemiological or animal data that can be used for quantitative risk estimates, the first main question is whether the compound should be regarded as genotoxic or not. In contrast to the policy of the US EPA, we have always considered this distinction to be vital, since low-dose risk extrapolations are only relevant for those carcinogens which apparently have a genotoxic mode of action. The theory of a mutational origin of tumour initiation is the basis for the simplified view that even at very low exposure levels there may be a risk, although infinitely small. This, in turn, is the basis for accepting low-dose extrapolation as a means of estimating the risk quantitatively. A threshold is assumed for other carcinogens that act at later stages in the tumour process, for example as tumour promoters, or in cases where the tumours can be expected to develop secondarily to cytotoxic damage. In practice, it is very diffucult to establish the mode of action for carcinogens, and many compounds show ambiguous results in different genotoxicity tests. Some events, like hormonal effects and effects through signal transduction, may also appear after exposure to very low doses. Still, we have only applied low-dose risk extrapolation for some genotoxic compounds (or metabolites). The recommended guideline values -the so-called low-risk levels -were in these cases set at the concentration that theoretically would result in an incre...