No abstract

Exposure to ambient particulate matter (PM) has been linked to several adverse health effects. Since vehicular traffic is a PM source of growing importance, we sampled total suspended particulate (TSP), PM(10), and PM(2.5) at six urban locations with pronounced differences in traffic intensity. The mutagenicity, DNA-adduct formation, and induction of oxidative DNA damage by the samples were studied as genotoxicological parameters, in relation to polycyclic aromatic hydrocarbon (PAH) levels, elemental composition, and radical-generating capacity (RGC) as chemical characteristics. We found pronounced differences in the genotoxicity and chemical characteristics of PM from the various locations, although we could not establish a correlation between traffic intensity and any of these characteristics for any of the PM size fractions. Therefore, the differences between locations may be due to local sources of PM, other than traffic. The concentration of total (carcinogenic) PAHs correlated positively with RGC, direct and S9-mediated mutagenicity, as well as the induction of DNA adducts and oxidative DNA damage. The interaction between total PAHs and transition metals correlated positively with DNA-adduct formation, particularly from the PM(2.5) fraction. RGC was not associated with one specific PM size fraction, but mutagenicity and DNA reactivity after metabolic activation were relatively high in PM(10) and PM(2.5), when compared with TSP. We conclude that the toxicological characteristics of urban PM samples show pronounced differences, even when PM concentrations at the sample sites are comparable. This implies that emission reduction strategies that take chemical and toxicological characteristics of PM into account may be useful for reducing the health risks associated with PM exposure.

In a rural area widespread pollution of friable and non-friable waste products was present, used to harden dirt tracks, yards, and driveways during . Exposure to environmental asbestos was assessed by a site approach, based on number of polluted sites within postal code areas, and by a household approach, based on number of households in the close vicinity to polluted sites within postal code areas. Based on asbestos soil investigations, 293 sites were identified with asbestos waste material at the surface, of which 77% contained crocidolite fibres as well as chrysotile fibres. The 293 sitesat-risk varied from 5 m 2 to 2722 m 2 and were surrounded by 347 households within 100 m of these sites. Distance to the plant was associated with the number of sites (r ¼ 0.36), and with the number of households (r ¼ 0.52). However, categorization of postal code areas into low, intermediate or high likelihood of exposure to asbestos showed a modest agreement between the site and household approach. In the site approach a total of 2.3 million person-years at risk were estimated with an average exposure of 1674 fibres/m 3 and an expected 1.8 cases of malignant mesothelioma each year. The household approach resulted in estimates of 1.2 million person-years at risk, and 0.9 cases of malignant mesothelioma per year, respectively. This study illustrates that asbestos waste on the surface of roads and yards in an area with over 130,000 inhabitants may result in long-term exposure to asbestos that will cause several cases of malignant mesothelioma each year. Although distance to plant, number of polluted sites and number of exposed household were associated, the modest agreement among these measures of exposure indicate that the exposure assessment strategy chosen in a particular study may result in considerable misclassification. Without detailed information on individual behaviour within the polluted area, it is difficult to show that a more individually oriented approach will perform better than an ecological approach.