BACKGROUND Substantial policy changes to control obesity, limit chronic disease, and reduce air pollution emissions, including greenhouse gasses, have been recommended. Transportation and planning policies that promote active travel by walking and cycling can contribute to these goals, potentially yielding further co-benefits. Little is known, however, about the interconnections among effects of policies considered, including potential unintended consequences. OBJECTIVES AND METHODS We review available literature regarding health impacts from policies that encourage active travel in the context of developing health impact assessment (HIA) models to help decision-makers propose better solutions for healthy environments. We identify important components of HIA models of modal shifts in active travel in response to transport policies and interventions. RESULTS AND DISCUSSION Policies that increase active travel are likely to generate large individual health benefits through increases in physical activity for active travelers. Smaller, but population-wide benefits could accrue through reductions in air and noise pollution. Depending on conditions of policy implementations, risk tradeoffs are possible for some individuals who shift to active travel and consequently increase inhalation of air pollutants and exposure to traffic injuries. Well-designed policies may enhance health benefits through indirect outcomes such as improved social capital and diet, but these synergies are not sufficiently well understood to allow quantification at this time. CONCLUSION Evaluating impacts of active travel policies is highly complex; however, many associations can be quantified. Identifying health-maximizing policies and conditions requires integrated HIAs.

This study demonstrates a simple method to estimate the extent to which the exposure of cyclists to NO(2) is reduced by using off-road cycle routes rather than on-road cycle routes. Diffusion tubes were used to measure monthly NO(2) concentrations on three paired sets of on- and off-road cycle journeys in and around the City of York in August and September 2008. These measurements were combined with estimates of journey times to calculate time-weighted average concentration and exposure on each route. The average concentration of NO(2) was significantly reduced by a mean of 37.5% when off-road routes were used in place of on-road routes and, despite the longer journey times for off-road routes, exposure was also significantly reduced by a mean of 25.5%. The method described in this study could be adopted more widely to provide a cost effective and simple means of assessing the benefits of alternative cycle routes that are provided by Local Authorities.

HASH(0x2acd2dfbdc60)

OBJECTIVES Monitoring studies have shown that commuters are exposed to high air pollution concentrations, but there is limited evidence of associated health effects. We carried out a study to investigate the acute respiratory health effects of air pollution related to commuting by bicycle. METHODS Twelve healthy adults cycled a low- and a high-traffic intensity route during morning rush hour in Utrecht, The Netherlands. Exposure to traffic-related air pollution was characterised by measurements of PM(10), soot and particle number. Before, directly after and 6 h after cycling we measured lung function (FEV(1), FVC, PEF), exhaled NO (FE(NO)) and respiratory symptoms. The association between post- minus pre-exposure difference in health effects and exposure during cycling was evaluated with linear regression models. RESULTS The average particle number concentration was 59% higher, while the average soot concentration was 39% higher on the high-traffic route than on the low-traffic route. There was no difference for PM(10). Contrary to our hypothesis, associations between air pollution during cycling and lung function changes immediately after cycling were mostly positive. Six hours after cycling, associations between air pollution exposure and health were mostly negative for lung function changes and positive for changes in exhaled NO, although non-significant. CONCLUSIONS We found substantial differences in ultrafine particle number and soot exposure between two urban cycling routes. Exposure to ultrafine particles and soot during cycling was weakly associated with increased exhaled NO, indicative of airway inflammation, and decrements in lung function 6 h after exposure. A limitation of the study was the relatively small sample size.

BACKGROUND Short-term exposure to air pollution has been associated with changes in blood pressure (BP) and emergency department visits for hypertension, but little is known about the effects of long-term exposure to traffic-related air pollution on BP and hypertension. OBJECTIVES We studied whether long-term exposure to air pollution is associated with BP and hypertension. METHODS In 1993-1997, 57,053 participants 50-64 years of age were enrolled in a population-based cohort study. Systolic and diastolic BP (SBP and DBP, respectively) were measured at enrollment. Self-reported incident hypertension during a mean follow-up of 5.3 years was assessed by questionnaire. We used a validated dispersion model to estimate residential long-term nitrogen oxides (NO(x)), a marker of traffic-related air pollution, for the 1- and 5-year periods prior to enrollment and before a diagnosis of hypertension. We conducted a cross-sectional analysis of associations between air pollution and BP at enrollment with linear regression, adjusting for traffic noise, measured short-term NO(x), temperature, relative humidity, and potential lifestyle confounders (n = 44,436). We analyzed incident hypertension with Cox regression, adjusting for traffic noise and potential confounders. RESULTS A doubling of NO(x) exposure during 1- and 5-year periods preceding enrollment was associated with 0.53-mmHg decreases [95% confidence interval (CI):-0.88,-0.19 mmHg] and 0.50-mmHg decreases (95% CI:-0.84,-0.16 mmHg) in SBP, respectively. Long-term exposure also was associated with a lower prevalence of baseline self-reported hypertension (per doubling of 5-year mean NO(x): odds ratio = 0.96; 95% CI: 0.91, 1.00), whereas long-term NO(x) exposure was not associated with incident self-reported hypertension during follow-up. CONCLUSIONS Long-term exposure to traffic-related air pollution was associated with a slightly lower prevalence of BP at baseline, but was not associated with incident hypertension.

OBJECTIVE Animal and cross-sectional epidemiological studies suggest a link between air pollution and diabetes, whereas the limited prospective data show mixed results. We studied the association between long-term exposure to traffic-related air pollution and incidence of diabetes. RESEARCH DESIGN AND METHODS We followed 57,053 participants of the Danish Diet, Cancer, and Health cohort in the Danish National Diabetes Register between baseline (1993-1997) and 27 June 2006. We estimated the mean levels of nitrogen dioxide (NO(2)) at the residential addresses of the cohort participants since 1971 and modeled the association between NO(2) and diabetes incidence with a Cox regression model, separately for two definitions of diabetes: all cases and a more strict definition where unconfirmed cases were excluded. RESULTS Over a mean follow-up of 9.7 years of 51,818 eligible subjects, there were 4,040 (7.8%) incident diabetes cases in total and 2,877 (5.5%) with confirmed diagnoses. Air pollution was not associated with all diabetes cases (hazard ratio 1.00 [95% CI 0.97-1.04] per interquartile range of 4.9 μg/m(3) mean NO(2) levels since 1971), but a borderline statistically significant association was detected with confirmed cases of diabetes (1.04 [1.00-1.08]). Among confirmed diabetes cases, effects were significantly enhanced in nonsmokers (1.12 [1.05-1.20]) and physically active people (1.10 [1.03-1.16]). CONCLUSIONS Long-term exposure to traffic-related air pollution may contribute to the development of diabetes, especially in individuals with a healthy lifestyle, nonsmokers, and physically active individuals.

BACKGROUND AND PURPOSE Years of exposure to tobacco smoke substantially increase the risk for stroke. Whether long-term exposure to outdoor air pollution can lead to stroke is not yet established. We examined the association between long-term exposure to traffic-related air pollution and incident and fatal stroke in a prospective cohort study. METHODS We followed 57,053 participants of the Danish Diet, Cancer and Health cohort in the Hospital Discharge Register for the first-ever hospital admission for stroke (incident stroke) between baseline (1993-1997) and 2006 and defined fatal strokes as death within 30 days of admission. We associated the estimated mean levels of nitrogen dioxide at residential addresses since 1971 to incident and fatal stroke by Cox regression analyses and examined the effects by stroke subtypes: ischemic, hemorrhagic, and nonspecified stroke. RESULTS Over a mean follow-up of 9.8 years of 52,215 eligible subjects, there were 1984 (3.8%) first-ever (incident) hospital admissions for stroke of whom 142 (7.2%) died within 30 days. We detected borderline significant associations between mean nitrogen dioxide levels at residence since 1971 and incident stroke (hazard ratio, 1.05; 95% CI, 0.99-1.11, per interquartile range increase) and stroke hospitalization followed by death within 30 days (1.22; 1.00-1.50). The associations were strongest for nonspecified and ischemic strokes, whereas no association was detected with hemorrhagic stroke. CONCLUSIONS Long-term exposure to traffic-related air pollution may contribute to the development of ischemic but not hemorrhagic stroke, especially severe ischemic strokes leading to death within 30 days.

BACKGROUND Exposure to air pollution in early life contributes to the burden of childhood asthma, but it is not clear whether long-term exposure to air pollution can lead to asthma onset or progression in adulthood. OBJECTIVES The authors studied the effect of exposure to traffic-related air pollution over 35 years on the risk for asthma hospitalisation in older people. METHODS 57 053 participants in the Danish Diet, Cancer and Health cohort, aged 50-65 years at baseline (1993-1997), were followed up for first hospital admission for asthma until 2006, and the annual nitrogen dioxide (NO(2)) levels were estimated as a proxy of the exposure to traffic-related air pollution at the residential addresses of the participants since 1971. The association between NO(2) and hospitalisation for asthma was modelled using Cox regression, for the full cohort and in people with and without previous hospitalisations for asthma, and the effect modification by comorbid conditions was assessed. RESULTS During 10.2 years' median follow-up, 977 (1.9%) of 53 695 eligible people were admitted to hospital for asthma: 821 were first-ever admissions and 176 were readmissions. NO(2) levels were associated with risk for asthma hospitalisation in the full cohort (HR and 95% CI per IQR, 5.8 μg/m(3): 1.12; 1.04-1.22), and for first-ever admissions (1.10; 1.01-1.20), with the highest risk in people with a history of asthma (1.41; 1.15-2.07) or chronic obstructive pulmonary disease (COPD)(1.30; 1.07-1.52) hospitalisation. CONCLUSIONS Long-term exposure to traffic-related air pollution increases the risk for asthma hospitalisation in older people. People with previous asthma or COPD hospitalisations are most susceptible.

BACKGROUND Vehicle engine exhaust includes ultrafine particles with a large surface area and containing absorbed polycyclic aromatic hydrocarbons, transition metals and other substances. Ultrafine particles and soluble chemicals can be transported from the airways to other organs, such as the liver, kidneys, and brain. Our aim was to investigate whether air pollution from traffic is associated with risk for other cancers than lung cancer. METHODS We followed up 54,304 participants in the Danish Diet Cancer and Health cohort for 20 selected cancers in the Danish Cancer Registry, from enrolment in 1993-1997 until 2006, and traced their residential addresses from 1971 onwards in the Central Population Registry. We used modeled concentration of nitrogen oxides (NO(x)) and amount of traffic at the residence as indicators of traffic-related air pollution and used Cox models to estimate incidence rate ratios (IRRs) after adjustment for potential confounders. RESULTS NO(x) at the residence was significantly associated with risks for cervical cancer (IRR, 2.45; 95% confidence interval [CI], 1.01;5.93, per 100 μg/m(3) NO(x)) and brain cancer (IRR, 2.28; 95% CI, 1.25;4.19, per 100 μg/m(3) NO(x)). CONCLUSIONS This hypothesis-generating study indicates that traffic-related air pollution might increase the risks for cervical and brain cancer, which should be tested in future studies.

BACKGROUND Previous studies have shown associations between air pollution and risk for lung cancer. OBJECTIVE We investigated whether traffic and the concentration of nitrogen oxides (NOx) at the residence are associated with risk for lung cancer. METHODS We identified 592 lung cancer cases in the Danish Cancer Registry among 52,970 members of the Diet, Cancer and Health cohort and traced residential addresses from 1 January 1971 in the Central Population Registry. We calculated the NOx concentration at each address by dispersion models and calculated the time-weighted average concentration for all addresses for each person. We used Cox models to estimate incidence rate ratios (IRRs) after adjustment for smoking (status, duration, and intensity), environmental tobacco smoke, length of school attendance, occupation, and dietary intake of fruit. RESULTS For the highest compared with the lowest quartile of NOx concentration at the residence, we found an IRR for lung cancer of 1.30 [95% confidence interval (CI), 1.05-1.61], and the IRR for lung cancer in association with living within 50 m of a major road (>10,000 vehicles/day) was 1.21 (95% CI, 0.95-1.55). The results showed tendencies of stronger associations among nonsmokers, among those with a relatively low fruit intake, and among those with a longer school attendance; only length of school attendance modified the effect significantly. CONCLUSIONS This study supports that risk for lung cancer is associated with different markers of air pollution from traffic near the residence.

RATIONALE Short-term exposure to air pollution has been associated with exacerbation of chronic obstructive pulmonary disease (COPD), whereas the role of long-term exposures on the development of COPD is not yet fully understood. OBJECTIVES We assessed the effect of exposure to traffic-related air pollution over 35 years on the incidence of COPD in a prospective cohort study. METHODS We followed 57,053 participants in the Danish Diet, Cancer, and Health cohort in the Hospital Discharge Register for their first hospital admission for COPD between 1993 and 2006. We estimated the annual mean levels of nitrogen dioxide (NO₂) and nitrogen oxides (NO(x)) at all residential addresses of the cohort participants since 1971 to an event or 2006 and used indicators of traffic near the residential address at recruitment. We assessed the association between exposure to air pollution and COPD incidence by Cox regression analyses for the full cohort, and for participants with and without comorbid conditions, including asthma, diabetes, or cardiovascular disease. MEASUREMENTS AND MAIN RESULTS A first hospital admission for COPD was recorded for 1,786 (3.4%) of 52,799 eligible subjects between recruitment (1993-1997) and 2006. COPD incidence was associated with the 35-year mean NO₂ level (hazard ratio, 1.08; 95% confidence interval, 1.02-1.14, per interquartile range of 5.8 μg/m³), with stronger associations in subjects with diabetes (1.29; 1.05-1.50) and asthma (1.19; 1.03-1.38). CONCLUSIONS Long-term exposure to traffic-related air pollution may contribute to the development of COPD with possibly enhanced susceptibility in people with diabetes and asthma.

HASH(0x24f858c0)

Current aerobiological research applies the hypothesis that the main source of atmospheric birch (Betula) pollen is forest trees. Our results indicate that the measured levels in Copenhagen are not only due to birch trees in Danish forests but that the urban areas also seem to be a significant source of birch pollen. A number of episodes in 2003 with enhanced pollen levels in Copenhagen seem to be associated with parks and gardens inside and just outside the city. Our results also indicate one long-range transport episode from remote sources in Poland and Germany. Finally, our results show that the pollen levels vary considerably over the day and geographically between Copenhagen and the city of Roskilde, 40 km away. We suggest, that these differences in time and space in the pollen levels are mapped using an integrated monitoring strategy.

The particle formation and growth events observed at a semirural background site in Denmark were analyzed based on particle number size distribution data collected during the period from February 2005 to December 2010. The new particle formation (NPF) events have been classified visually in detail according to 3D daily plots in combination with an automatic routine. A clear seasonal variation was found in the way that events occurred more frequently during the warm season from May to September and especially in June. The mean values of the apparent 6 nm particle formation rates, the growth rate and the condensation sink were about 0.36 cm(-3) s(-1), 2.6 nm h(-1), 4.3 × 10(-3) s(-1), respectively. A positive relationship of oxidation capacity (O(X) = O(3) + NO(2)) of the atmosphere and the appearance of NPF events was found indicating that the oxidation of the atmosphere was linked to the formation of new particles. An analysis of a 3-day backward trajectories revealed that NW air masses from the North Sea were giving the highest probability of NPF events, namely between 20 and 40 %.

This study presents a methodological scheme developed to provide a combined air and noise pollution exposure assessment based on measurements from personal portable monitors. Provided that air and noise pollution are considered in a co-exposure approach, they represent a significant environmental hazard to public health. The methodology is demonstrated for the city of Thessaloniki, Greece. The results of an extensive field campaign are presented and the variations in personal exposure between modes of transport, routes, streets and transport microenvironments are evaluated. Air pollution and noise measurements were performed simultaneously along several commuting routes, during the morning and evening rush hours. Combined exposure to environmental pollutants is highlighted based on the Combined Exposure Factor (CEF) and Combined Dose and Exposure Factor (CDEF). The CDEF takes into account the potential relative uptake of each pollutant by considering the physical activities of each citizen. Rather than viewing environmental pollutants separately for planning and environmental sustainability considerations, the possibility of an easy-to-comprehend co-exposure approach based on these two indices is demonstrated. Furthermore, they provide for the first time a combined exposure assessment to these environmental pollutants for Thessaloniki and in this sense they could be of importance for local public authorities and decision makers. A considerable environmental burden for the citizens of Thessaloniki, especially for VOCs and noise pollution levels is observed. The material herein points out the importance of measuring public health stressors and the necessity of considering urban environmental pollution in a holistic way.

The exposure of citizens to elevated air pollution concentrations is one of the major factors leading to the deterioration of the quality of life and possibly to health problems in urban areas. The concentration of air pollutants depends largely on pollutant emission levels. If the statistical probability distribution function of the concentration of an air pollutant is known, it is possible to estimate how many times this concentration exceeds the air quality standards, or estimate changes in the emission levels in an area. It can be also used to estimate the long term exposure of population to certain pollutants. In this paper fifteen theoretical probability distribution functions, were used to fit the actual concentration frequency distributions of CO, NO(2), O(3,) SO(2), and Black Smoke (BS) in Athens, Greece for a 23-year period. The results showed that the theoretical distribution type best describing the distribution of the pollutants is Inverse Gaussian followed by the Extreme value distribution. The number of exceedances of air quality limits was used to validate the performance of the theoretical distributions that were best fitted to the observed ones. The temporal evolution of emission strength was estimated through the temporal evolution of the parameters of the probability distribution functions. Missing periods were accounted for by estimating the respective distribution functions through interpolation or extrapolation from the existing ones. The derived variation of emission levels consistently represents the emission reduction strategies enforced over the years, as well as the escalating growth of the passenger car fleet volume, and could be a useful tool for the design and assessment of emission control strategies.

The aim of this study was to evaluate the impact of urban air pollution, assessed through reliable indicators of exposure, on asthma and allergies in schoolchildren.A validated dispersion model, combining data on traffic conditions, topography, meteorology and background pollution was used to relate three-years-averaged concentrations of major urban pollutants at the schools' address to skin prick test, exercise-induced asthma, and reported asthma and allergies in 6683 children (9-11 years), attending 108 schools randomly selected in six French communities.For the 4907 children having resided at their current address in the past three years, asthma (exercised-induced, past year and lifetime) was significantly positively associated with benzene, SO2, PM10, NOx and CO, eczema (lifetime and past year) with benzene, PM10, NO2, NOx and CO, lifetime allergic rhinitis with PM10 and sensitisation to pollens with benzene and PM10. Among the 2213 children residing at their current address since birth, the associations persisted for lifetime asthma with benzene (adjusted odds ratio per interquartile range (95% confidence interval)=1.3 (1.0-1.9)) and PM10 (1.4 (1.0-2.0)) and for sensitisation to pollens with VOC (1.3 (1.0-1.9)) and PM10 (1.2 (1.0-1.9)).Accurately modelled urban air pollution was associated with some measures of childhood asthma and allergies.

The Brooklyn Traffic Real-Time Ambient Pollutant Penetration and Environmental Dispersion (B-TRAPPED) field study examined indoor and outdoor exposure to traffic-generated air pollution by studying the individual processes of generation of traffic emissions, transport and dispersion of air contaminants along a roadway, and infiltration of the contaminants into a residence. Real-time instrumentation was used to obtain highly resolved time-series concentration profiles for a number of air pollutants. The B-TRAPPED field study was conducted in the residential Sunset Park neighborhood of Brooklyn, NY, USA, in May 2005. The neighborhood contained the Gowanus Expressway (Interstate 278), a major arterial road (4(th) Avenue), and residential side streets running perpendicular to the Gowanus Expressway and 4(th) Avenue. Synchronized measurements were obtained inside a test house, just outside the test house façade, and along the urban residential street canyon on which the house was located. A trailer containing Federal Reference Method (FRM) and real-time monitors was located next to the Gowanus Expressway to assess the source. Ultrafine particulate matter (PM), PM(2.5), nitrogen oxides (NO(x)), sulfur dioxide (SO(2)), carbon monoxide (CO), carbon dioxide (CO(2)), temperature, relative humidity, and wind speed and direction were monitored. Different sampling schemes were devised to focus on dispersion along the street canyon or infiltration into the test house. Results were obtained for ultrafine PM, PM(2.5), criteria gases, and wind conditions from sampling schemes focused on street canyon dispersion and infiltration. For comparison, the ultrafine PM and PM(2.5) results were compared with an existing data set from the Los Angeles area, and the criteria gas data were compared with measurements from a Vancouver epidemiologic study. Measured ultrafine PM and PM(2.5) concentration levels along the residential urban street canyon and at the test house façade in Sunset Park were demonstrated to be comparable to traffic levels at an arterial road and slightly higher than those in a residential area of Los Angeles. Indoor ultrafine PM levels were roughly 3-10 times lower than outdoor levels, depending on the monitor location. CO, NO(2), and SO(2) levels were shown to be similar to values that produced increased risk of chronic obstructive pulmonary disease hospitalizations in the Vancouver studies.

Personal exposures to fine particulate matter air pollution (PM(2.5)), and to its traffic-related fraction, were investigated in a group of urban children with asthma. The relationships of personal and outdoor school-site measurements of PM(2.5) and elemental carbon (EC) were characterized for a total of 40 fifth-grade children. These students, from four South Bronx, NY schools, each carried air pollution monitoring equipment with them for 24 h per day for approximately 1 month. Daily EC concentrations were estimated using locally calibrated reflectance of the PM(2.5) samples. Personal EC concentration was more closely related to outdoor school-site EC (median subject-specific: r=0.64) than was personal PM(2.5) to school-site PM(2.5) concentration (median subject-specific: r=0.33). Regression models also showed a stronger, more robust association of school site with personal measurements for EC than those for PM(2.5). High traffic pollution exposure was found to coincide with the weekday early morning rush hour, with higher personal exposures for participants living closer to a highway (<500 ft). A significant linear relationship of home distance from a highway with personal EC pollution exposure was also found (up to 1000 ft). This supports the assumptions by previous epidemiological studies using distance from a highway as an index of traffic PM exposure. These results are also consistent with the assumption that traffic, and especially smoke emitted from diesel vehicles, is a significant contributor to personal PM exposure levels in children living in urban areas such as the South Bronx, NY.

Vehicle exhaust emissions are a dominant feature of urban environments and are widely believed to have detrimental effects on plants. The effects of diesel exhaust emissions on 12 herbaceous species were studied with respect to growth, flower development, leaf senescence and leaf surface wax characteristics. A diesel generator was used to produce concentrations of nitrogen oxides (NO(x)) representative of urban conditions, in solardome chambers. Annual mean NO(x) concentrations ranged from 77 nl l(-l) to 98 nl l(-1), with NO:NO(2) ratios of 1.4-2.2, providing a good experimental simulation of polluted roadside environments. Pollutant exposure resulted in species-specific changes in growth and phenology, with a consistent trend for accelerated senescence and delayed flowering. Leaf surface characteristics were also affected; contact angle measurements indicated changes in surface wax structure following pollutant exposure. The study demonstrated clearly the potential for realistic levels of vehicle exhaust pollution to have direct adverse effects on urban vegetation.

A previous investigation into methods of exposure reduction for the pedestrian in the urban commuter environment highlighted the impact of a low boundary wall on the dispersion of air pollutants from adjacent traffic sources. The impact of low boundary walls on the dispersion of air pollutants in street canyons has been brought forward in this investigation to examine them, in more generic terms, with a view to highlighting exposure reduction strategies for pedestrians. 3D Computational Fluid Dynamics (CFD) models were used to examine this effect for varying wind speeds and directions in different street canyon geometries. The results of this investigation show that a low boundary wall located at the central median of the street canyon creates a significant reduction in pedestrian exposure on the footpath. Reductions of up to 40% were found for perpendicular wind directions and up to 75% for parallel wind directions, relative to the same canyon with no wall. The magnitude of the exposure reduction was also found to vary according to street canyon geometry and wind speed.

BACKGROUND Both air and noise pollution associated with motor vehicle traffic have been associated with cardiovascular disease. Similarities in pollution source and health outcome mean that there is potential for noise to confound studies of air pollution and cardiovascular disease, and vice versa, or for more complex interactions to occur. METHODS The correlations between 2-week average roadside concentrations of nitrogen dioxide (NO(2)) and nitrogen oxides (NO(X)) and short term average noise levels (L(eq,5min)) for 103 urban sites with varying traffic, environment and infrastructure characteristics were examined. RESULTS The Pearson correlation coefficient for L(eq,5min) and NO(2) was 0.53, and for L(eq,5min) and NO(X), 0.64. Factors influencing the degree of correlation were number of lanes on the closest road, number of cars or trucks during noise sampling and presence of a major intersection. CONCLUSIONS We recommend measurement of both pollutants in future studies of traffic-related pollution and cardiovascular disease to allow for more sophisticated analysis of this relationship.

ABSTRACT: BACKGROUND: Exposure to air pollution particles has been acknowledged to be associated with excess generation of oxidative damage to DNA in experimental model systems and humans. The use of standard reference material (SRM), such as SRM1650 and SRM2975, is advantageous because experiments can be reproduced independently, but exposure to such samples may not mimic the effects observed after exposure to authentic air pollution particles. This study was designed to compare the DNA oxidizing effects of authentic street particles with SRM1650 and SRM2975. The authentic street particles were collected at a traffic intensive road in Copenhagen, Denmark. RESULTS: All of the particles generated strand breaks and oxidized purines in A549 lung epithelial cells in a dose-dependent manner and there were no overt differences in their potency. The exposures also yielded dose-dependent increase of cytotoxicity (as lactate dehydrogenase release) and reduced colony forming ability with slightly stronger cytotoxicity of SRM1650 than of the other particles. In contrast, only the authentic street particles were able to generate 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) in calf thymus DNA, which might be due to the much higher level of transition metals. CONCLUSION: Authentic street particles and SRMs differ in their ability to oxidize DNA in a cell-free environment, whereas cell culture experiments indicate that the particle preparations elicit a similar alteration of the level of DNA damage and small differences in cytotoxicity. Although it cannot be ruled out that SRMs and authentic street particles might elicit different effects in animal experimental models, this study indicates that on the cellular level, SRM1650 and SRM2975 are suitable surrogate samples for the study of authentic street particles.

A novel methodological design comprising multilevel assessments of exposures of examinees to controlled ambient air pollution according to the data of route stations was developed to examine the population of large towns. The design was tested in 4 surveys of Moscow residents (apparently healthy and outpatients with a number of chronic diseases). The findings indicate the fundamental possibility of altering the traditional differential design of biomedical surveys of the population, by introducing more evidence-based regression analyses and dividing the contributions of individual chemicals to the observed changes in health indices.