Quantifying the impact of air pollution on the public’s health has become an increasingly critical component in policy discussion. Recent data indicate that more than 70% of the world population lives in cities. Several studies reported that current levels of air pollutants in urban areas are associated with adverse health risks, namely, cardiovascular diseases and lung cancer. IARC recently classified outdoor air pollution and related particulate matter (PM) as carcinogenic to humans. Despite the air quality improvements observed over the last few years, there is still continued widespread exceedance within Europe, particularly regarding PM and nitrogen oxides (NOx). The European Air Quality Directive 2008/50/EC requires Member States to design appropriate air quality plans for zones where air quality does not comply with established limit values. However, in most cases, air quality is only quantified using a combination of monitored and modeled data and no health impact assessment is carried out. An integrated approach combining the effects of several emission abatement measures on air quality, impacts on human health, and associated implementation costs enables an effective cost–benefit analysis and an added value to the decision-making process. Hence, this review describes the basic steps and tools for integrating health into air quality assessment (health indicators, exposure-response functions). In addition, consideration is given to two major outdoor pollutants: PM and NO₂. A summary of the health metrics used to assess the health impact of PM and NO₂ and recent epidemiologic data are also described.

The comet assay has become a popular method for the assessment of DNA damage in biomonitoring studies and genetic toxicology. However, few studies have addressed the issue of the noted inter-laboratory variability of DNA damage measured by the comet assay. In this study, 12 laboratories analysed the level of DNA damage in monocyte-derived THP-1 cells by either visual classification or computer-aided image analysis of pre-made slides, coded cryopreserved samples of cells and reference standard cells (calibration curve samples). The reference standard samples were irradiated with ionizing radiation (0–10 Gy) and used to construct a calibration curve to calculate the number of lesions per 10⁶ base pair. All laboratories detected dose–response relationships in the coded samples irradiated with ionizing radiation (1.5–7 Gy), but there were overt differences in the level of DNA damage reported by the different laboratories as evidenced by an inter-laboratory coefficient of variation (CV) of 47%. Adjustment of the primary comet assay end points by a calibration curve prepared in each laboratory reduced the CV to 28%, a statistically significant reduction (P < 0.05, Levene's test). A large fraction of the inter-laboratory variation originated from differences in image analysis, whereas the intra-laboratory variation was considerably smaller than the variation between laboratories. In summary, adjustment of primary comet assay results by reference standards reduces inter-laboratory variation in the level of DNA damage measured by the alkaline version of the comet assay.

DNA damage is commonly measured at the level of individual cells using the so-called comet assay (single-cell gel electrophoresis). As the frequency of DNA breaks increases, so does the fraction of the DNA extending towards the anode, forming the comet tail. Comets with almost all DNA in the tail are often referred to as ‘hedgehog’ comets and are widely assumed to represent apoptotic cells. We review the literature and present theoretical and empirical arguments against this interpretation. The level of DNA damage in these comets is far less than the massive fragmentation that occurs in apoptosis. ‘Hedgehog’ comets are formed after moderate exposure of cells to, for example, H₂O₂, but if the cells are incubated for a short period, ‘hedgehogs’ are no longer seen. We confirm that this is not because DNA has degraded further and been lost from the gel, but because the DNA is repaired. The comet assay may detect the earliest stages of apoptosis, but as it proceeds, comets disappear in a smear of unattached DNA. It is clear that ‘hedgehogs’ can correspond to one level on a continuum of genotoxic damage, are not diagnostic of apoptosis and should not be regarded as an indicator of cytotoxicity.