Background

Although the dispersion model approach has been used in some epidemiologic studies to examine health effects of traffic-specific air pollution, no study has evaluated the model predictions vigorously.

Methods

We evaluated total and traffic-specific particulate matter < 10 and < 2.5 μm in aero-dynamic diameter (PM₁₀, PM_2.5), nitrogren dioxide, and nitrogen oxide concentrations predicted by Gaussian dispersion models against fixed-site measurements at different locations, including traffic-impacted, urban-background, and alpine settings between and across cities. The model predictions were then used to estimate individual subjects’ historical and cumulative exposures with a temporal trend model.

Results

Modeled PM₁₀ and NO₂ predicted at least 55% and 72% of the variability of the measured PM₁₀ and NO₂, respectively. Traffic-specific pollution estimates correlated with the NO_x measurements (R ≥0.77) for background sites but not for traffic sites. Regional background PM₁₀ accounted for most PM₁₀ mass in all cities. Whereas traffic PM₁₀ accounted for < 20% of the total PM₁₀, it varied significantly within cities. The modeling error for PM₁₀ was similar within and between cities. Traffic NO_x accounted for the majority of NO_x mass in urban areas, whereas background NO_x accounted for the majority of NO_x in rural areas. The within-city NO₂ modeling error was larger than that between cities.

Conclusions

The dispersion model predicted well the total PM₁₀, NO_x, and NO₂ and traffic-specific pollution at background sites. However, the model underpredicted traffic NO_x and NO₂ at traffic sites and needs refinement to reflect local conditions. The dispersion model predictions for PM₁₀ are suitable for examining individual exposures and health effects within and between cities.

Background

Heart rate variability (HRV), a measure of cardiac autonomic tone, has been associated with cardiovascular morbidity and mortality. Short-term studies have shown that subjects exposed to higher traffic-associated air pollutant levels have lower HRV.

Objective

Our objective was to investigate the effect of long-term exposure to nitrogen dioxide on HRV in the Swiss cohort Study on Air Pollution and Lung Diseases in Adults (SAPALDIA).

Methods

We recorded 24-hr electrocardiograms in randomly selected SAPALDIA participants ≥ 50 years of age. Other examinations included an interview investigating health status and measurements of blood pressure, body height, and weight. Annual exposure to NO₂ at the address of residence was predicted by hybrid models (i.e., a combination of dispersion predictions, land-use, and meteorologic parameters). We estimated the association between NO₂ and HRV in multivariable linear regression models. Complete data for analyses were available for 1,408 subjects.

Results

For women, but not for men, each 10-μg/m increment in 1-year averaged NO₂ level was associated with a decrement of 3% (95% CI, −4 to −1) for the standard deviation of all normal-to-normal RR intervals (SDNN), −6% (95% CI, −11 to −1) for nighttime low frequency (LF), and −5% (95% CI, −9 to 0) for nighttime LF/high-frequency (HF) ratio. We saw no significant effect for 24-hr total power (TP), HF, LF, or LF/HF or for nighttime SDNN, TP, or HF. In subjects with self-reported cardiovascular problems, SDNN decreased by 4% (95% CI, −8 to −1) per 10-μg/m increase in NO₂.

Conclusions

There is some evidence that long-term exposure to NO₂ is associated with cardiac autonomic dysfunction in elderly women and in subjects with cardiovascular disease.

Background

Whether there is a causal relation between long-term exposure to traffic and asthma development is so far not clear. This may be explained by inaccurate exposure assessment.

Objective

We investigated the associations of long-term traffic-related exposures with asthma onset assessed retrospectively and respiratory symptoms in 9- to 10-year-old children.

Methods

We collected information on respiratory outcomes and potential confounding variables by parental questionnaire in 2,871 children in Oslo. Nitrogen dioxide exposure was assessed by the EPISODE dispersion model and assigned at updated individual addresses during lifetime. Distance to major road was assigned at birth address and address by date of questionnaire. Cox proportional hazard regression and logistic regression were used.

Results

We did not find positive associations between any long-term traffic-related exposure and onset of doctor-diagnosed asthma. An interquartile range (IQR) increase of NO₂ exposure before asthma onset was associated with an adjusted risk ratio of 0.82 [95% confidence interval (CI), 0.67–1.02]. Handling early asthma cases (children < 4 years of age) with recovery during follow-up as noncases gave a less negative association. The associations for late asthma onset (≥ 4 years of age) were positive but not statistically significant. For current symptoms, an IQR increase of previous year’s NO₂ exposure was associated with adjusted odds ratios of 1.01 (95% CI, 0.83–1.23) for wheeze, 1.10 (95% CI, 0.79–1.51) for severe wheeze, and 1.01 (95% CI, 0.84–1.21) for dry cough.

Conclusions

We were not able to find positive associations of long-term traffic-related exposures with asthma onset or with current respiratory symptoms in 9- to 10-year-old children in Oslo.

The purpose of this study was to assess the effect of long-term ambient particulate matter (PM) on risk of fatal coronary heart disease (CHD). A cohort of 3,239 nonsmoking, non-Hispanic white adults was followed for 22 years. Monthly concentrations of ambient air pollutants were obtained from monitoring stations [PM < 10 μm in aerodynamic diameter (PM₁₀), ozone, sulfur dioxide, nitrogen dioxide] or airport visibility data [PM < 2.5 μm in aerodynamic diameter (PM_2.5)] and interpolated to ZIP code centroids of work and residence locations. All participants had completed a detailed lifestyle questionnaire at baseline (1976), and follow-up information on environmental tobacco smoke and other personal sources of air pollution were available from four subsequent questionnaires from 1977 through 2000. Persons with prevalent CHD, stroke, or diabetes at baseline (1976) were excluded, and analyses were controlled for a number of potential confounders, including lifestyle. In females, the relative risk (RR) for fatal CHD with each 10-μg/m increase in PM_2.5 was 1.42 [95% confidence interval (CI), 1.06–1.90] in the single-pollutant model and 2.00 (95% CI, 1.51–2.64) in the two-pollutant model with O₃. Corresponding RRs for a 10-μg/m increase in PM_10-2.5 and PM₁₀ were 1.62 and 1.45, respectively, in all females and 1.85 and 1.52 in postmenopausal females. No associations were found in males. A positive association with fatal CHD was found with all three PM fractions in females but not in males. The risk estimates were strengthened when adjusting for gaseous pollutants, especially O₃, and were highest for PM_2.5. These findings could have great implications for policy regulations.

Although the nephrotoxicity of uranium has been established through numerous animal studies, relatively little is known about the effects of long-term environmental uranium exposure. Using a combination of conventional biochemical studies and serial analysis of gene expression (SAGE), we examined the renal responses to uranyl nitrate (UN) chronic exposure. Renal uranium levels were significantly increased 4 months after ingestion of uranium in drinking water. Creatinine levels in serum were slightly but significantly increased compared with those in controls. Although no further significant differences in other parameters were noted, substantial molecular changes were observed in toxicogenomic profiles. UN induced dramatic alterations in expression levels of more than 200 genes, mainly up-regulated, including oxidative-response–related genes, genes encoding for cellular metabolism, ribosomal proteins, signal transduction, and solute transporters. Seven differentially expressed transcripts were confirmed by real-time quantitative polymerase chain reaction. In addition, significantly increased peroxide levels support the implication of oxidative stress in UN toxicant response. This report highlights the potential of SAGE for the discovery of novel toxicant-induced gene expression alterations. Here, we present, for the first time, a comprehensive view of renal molecular events after uranium long-term exposure.