Background: A few studies have investigated the interaction between exposure to road traffic noise, air pollutants, and cardiovascular disease (CVD), but their results were inconsistent. This cross-sectional study investigated whether road traffic noise, particulate matter with dynamic diameter less than 10 μm (PM₁₀) and nitrogen dioxides (NO₂) exposure were independently associated with the risk of CVD. Methods: We recruited 663 volunteers who had been living near main roads for more than three years in 2008. Information concerning the subjects’ home addresses was combined with noise measurements at 42 locations and annual average of air pollutants from 2 monitoring stations to estimate individual exposure. Multivariate logistic regression was used to calculate the odds ratio (OR) for diagnosed CVD, adjusting for potential confounders and co-exposure. Results: Only per 5-dBA increase in road traffic noise was significantly associated with elevated risk of CVD (adjusted OR = 2.23, 95% confidence interval (CI) = 1.26–3.93) in the single-exposure models. Such association was aggravated (adjusted OR = 2.96, 95% CI = 1.41–6.23) after adjustment for total traffic and PM₁₀ or NO₂ in the two-exposure models. Conclusions: Road traffic noise exposure may be associated with the increasing prevalence of CVD. No synergistic association was observed between co-exposure to noise and air pollutants and the risk of CVD.

Personal PM 2.5 data from two recent exposure studies, the Scripted Activity Study and the Older Adults Study, were used to develop models predicting 24-h personal PM 2.5 exposures. Both studies were conducted concurrently in the summer of 1998 and the winter of 1999 in Baltimore, MD. In the Scripted Activity Study, 1-h personal PM 2.5 exposures were measured. Data were used to identify significant factors affecting personal exposures and to develop 1-h personal exposure models for five different micro-environments. By incorporating the time-activity diary data, these models were then combined to develop a time-weighted microenvironmental personal model (model M1AD) to predict the 24-h PM 2.5 exposures measured for individuals in the Older Adults Study. Twenty-four-hour time-weighted models were also developed using 1-h ambient PM 2.5 levels and time-activity data (model A1AD) or using 24-h ambient PM 2.5 levels and time-activity data (model A24AD). The performance of these three models was compared to that using 24-h ambient concentrations alone (model A24). Results showed that factors affecting 1-h personal PM 2.5 exposures included air conditioning status and the presence of environmental tobacco smoke (ETS) for indoor micro-environments, consistent with previous studies. ETS was identified as a significant contributor to measured 24-h personal PM 2.5 exposures. Staying in an ETS-exposed microenvironment for 1 h elevated 24-h personal PM 2.5 exposures by approximately 4 w g/m 3 on average. Cooking and washing activities were identified in the winter as significant contributors to 24-h personal exposures as well, increasing 24-h personal PM 2.5 exposures by about 4 and 5 w g/m 3 per hour of activity, respectively. The ability of 3 microenvironmental personal exposure models to estimate 24-h personal PM 2.5 exposures was generally comparable to and consistently greater than that of model A24. Results indicated that using time-activity data with 1-h exposure information, either as micro-environment-specific exposures (model M1AD) or as ambient concentrations (model A1AD), improves our ability to estimate 24-h personal PM 2.5 exposure over the model using 24-h averaged ambient levels alone (model A24). Model performance was higher in the summer than in the winter season. In addition, higher crude R 2 values were reported for subjects participating in both seasons, where the R 2 values equaled .53, .55, .46, and .38 for models M1AD, A1AD, A24AD, and A24, respectively. The low predictive ability of the microenvironmental exposure models in the winter might, in part, be attributed to the narrow dynamic range of personal PM 2.5 exposures.

Environmental epidemiological studies have consistently reported associations between ambient particulate matter (PM) concentrations and everyday mortality/morbidity. Many urban dwellers in Asia live in high-rise apartment buildings; thus, the pollutant concentrations of their immediate outdoor environments are affected by the vertical distribution of pollutants in the atmosphere. The vertical distributions of pollutants provide unique information about their sources and dynamic transport in urban areas, as well as their relationship to people’s exposure at ground level, while the vertical distributions of pollutants have rarely been considered in exposure assessment. In the current study, PM concentrations (with aerodynamic diameters less than 1.0 μm (PM₁), 2.5 μm (PM_2.5), and 10 μm (PM₁₀)), nanoparticles, black carbon (BC), and particle-bound polycyclic aromatic hydrocarbons (p-PAHs) were measured at different residential heights—6 m, 16 m, and 27 m—at Feng Chia University near a popular night market in Western Taiwan. PM_2.5 data were further adopted for health risk estimations. In winter, the magnitude of PM₁, PM_2.5, and PM₁₀ concentrations were 16 m > 6 m > 27 m; nanoparticle concentrations were 6 m > 27 m > 16 m; and BC and p-PAHs concentrations were 27 m > 16 m > 6 m. In summer, PM₁, PM_2.5, and PM₁₀ concentrations ranged from 6 m > 16 m > 27 m; nanoparticle concentrations were 6 m > 16 m; and BC and p-PAHs concentrations were from 27 m > 16 m. PM and constituents concentrations during winter were significantly higher in the nighttime than those in daytime, and levels of PM₁, PM_2.5, and PM₁₀ increased rapidly on 6 m and 16 m heights (but did not increase at 27 m) after 5 pm, whereas these trends became less significant in summer. Health risk analysis for PM_2.5 concentrations showed a decrease in lung cancer mortality rate and an extended lifespan for residents living at 27 m. Overall, the current study investigated the vertical profile of particulate matters and analyzed health impacts of PM_2.5 at different residential heights in urban area of Taiwan. As the distributions of PM and the constituents varied at different residential heights, exposure and risk assessment of particle concentrations with multiple sizes and various components at broader vertical heights should be further investigated.

To evaluate the cardiovascular impact of traffic-related pollutant exposure on healthy young adults, the research team has collected the primary data of in-cabin exposure to air pollutants and heart rate variability (HRV). Twenty young healthy college students were recruited in Taipei metropolitan area. In addition to electrocardiogram, personal exposure to air pollutants, i.e., particulate matter (PM) and carbon monoxide (CO), and weather conditions, including temperature and relative humidity (RH), on campus, bus, and mass rapid transit were monitored continuously. The following HRV parameters were evaluated using generalized additive mixed model to adjust for personal and meteorological variables: heart rate (HR), the square root of the mean of the sum of the squares of differences between adjacent normal-to-normal (NN) intervals (r-MSSD), the standard deviation of all NN intervals (SDNN), the percentage of successive NN interval differences greater than 50 ms (pNN50), low-frequency power (LF), high-frequency power (HF), total power (TP), and LF/HF. They were assessed to find out the association between in-cabin exposure and HRV parameters. Compared with the HRV parameters measured on campus, the percent changes in r-MSSD, SDNN, pNN50+1, LF, HF, and TP decreased when the participants were in public transits. After adjusting for all locations, 5 min moving averages of PM_2.5–10 and PM₁ were significantly associated with the increase in the percent changes in HR and SDNN. Additionally, 5 min moving averages of PM_2.5–10 exposure were significantly associated with the decrease in the percent change in HF, while it was significantly associated with the increase of the percent change in LF/HF. The reduction of the percent change in HR was also found to be significantly associated with 5 min CO moving averages. To conclude, current analyses have shown that size-fractionated PMs and CO exposure in public transits might lead to significant changes of HRV parameters for healthy young adults.

As a non-invasive method, heart rate variability (HRV) has been widely used to study cardiovascular autonomous control. Environmental epidemiological studies indicated that the increase in an average concentration of particulate matter (PM) would result in a decrease in HRV, which was related to the increase of cardiovascular mortality in patients with myocardial infarction and the general population. With rapid economic and social development in Asia, how air pollutants, such as PM of different sizes and their components, affect the cardiovascular health of older people, still need to be further explored. The current study includes a 72 h personal exposure monitoring of seven healthy older people who lived in the Taipei metropolitan area. Mobile equipment, a portable electrocardiogram recorder, and the generalized additive mixed model (GAMM) were adopted to evaluate how HRV indices were affected by size-fractionated PM, particle-bound polycyclic aromatic hydrocarbons (p-PAHs), black carbon (BC), and carbon monoxide (CO). Other related confounding factors, such as age, sex, body mass index (BMI), temperature, relative humidity (RH), time, and monitoring week were controlled by fixed effects of the GAMM. Statistical analyses of multi-pollutant models showed that PM_2.5–10, PM₁, and nanoparticle (NP) could cause heart rate (HR), time-domain indices, and frequency-domain indices to rise; PM_1–2.5 and BC would cause the frequency-domain index to rise; p-PAHs would cause HR to rise, and CO would cause time-domain index and frequency-domain index to decline. In addition, the moving average time all fell after one hour and might appear at 8 h in HRVs’ largest percentage change caused by each pollutant, results of which suggested that size-fractionated PM, p-PAHs, BC, and CO exposures have delayed effects on HRVs. In conclusion, the results of the study showed that the increase in personal pollutant exposure would affect cardiac autonomic control function of healthy older residents in metropolitan areas, and the susceptibility of cardiovascular effects was higher than that of healthy young people. Since the small sample size would limit the generalizability of this study, more studies with larger scale are warranted to better understand the HRV effects of simultaneous PM and other pollution exposures for subpopulation groups.