Air pollution and traffic noise interact to affect cognitive health in older Mexican Americans.

BACKGROUND: Both air pollution and noise exposures have separately been shown to affect cognitive impairment. Here, we examine how air pollution and noise exposures interact to influence the development of incident dementia or cognitive impairment without dementia (CIND). METHODS: We used 1,612 Mexican American participants from the Sacramento Area Latino Study on Aging conducted from 1998 to 2007. Air pollution (nitrogen dioxides, particulate matter, ozone) and noise exposure levels were modeled with a land-use regression and via the SoundPLAN software package implemented with the Traffic Noise Model applied to the greater Sacramento area, respectively. Using Cox proportional hazard models, we estimated the hazard of incident dementia or CIND from air pollution exposure at the residence up to 5-years prior to diagnosis for the members of each risk set at event time. Further, we investigated whether noise exposure modified the association between air pollution exposure and dementia or CIND. RESULTS: In total, 104 incident dementia and 159 incident dementia/CIND cases were identified during the 10 years of follow-up. For each ∼2 µg/m3 increase in time-varying 1- and 5-year average PM2.5 exposure, the hazard of dementia increased 33% (HR = 1.33, 95%CI: 1.00, 1.76). The hazard ratios for NO2-related dementia/CIND and PM2.5-related dementia were stronger in high-noise (≥65 dB) exposed than low-noise (<65 dB) exposed participants. CONCLUSION: Our study indicates that PM2.5 and NO2 air pollution adversely affect cognition in elderly Mexican Americans. Our findings also suggest that air pollutants may interact with traffic-related noise exposure to affect cognitive function in vulnerable populations.

Ozone Exposure, Outdoor Physical Activity, and Incident Type 2 Diabetes in the SALSA Cohort of Older Mexican Americans.

BACKGROUND: Type 2 diabetes is a leading contributor to the global burden of morbidity and mortality. Ozone (O3) exposure has previously been linked to diabetes. OBJECTIVE: We studied the impact of O3 exposure on incident diabetes risk in elderly Mexican Americans and investigated whether outdoor physical activity modifies the association. METHODS: We selected 1,090 Mexican American participants from the Sacramento Area Latino Study on Aging conducted from 1998 to 2007. Ambient O3 exposure levels were modeled with a land-use regression built with saturation monitoring data collected at 49 sites across the Sacramento metropolitan area. Using Cox proportional hazard models, we estimated the risk of developing incident diabetes based on average O3 exposure modeled for 5-y prior to incident diabetes diagnosis or last follow-up. Further, we estimated outdoor leisure-time physical activity at baseline and investigated whether higher vs. lower levels modified the association between O3 exposure and diabetes. RESULTS: In total, 186 incident diabetes cases were identified during 10-y follow-up. Higher levels of physical activity were negatively associated with incident diabetes [hazard ratio (HR)=0.64 (95% CI: 0.43, 0.95)]. The estimated HRs for incident diabetes was 1.13 (95% CI: 1.00, 1.28) per 10-ppb increment of 5-y average O3 exposure; also, this association was stronger among those physically active outdoors [HR=1.52 (95% CI: 1.21, 1.90)], and close to null for those reporting lower levels of outdoor activity [HR=1.04 (95% CI: 0.90, 1.20), pinteraction=0.01]. CONCLUSIONS: Our findings suggest that ambient O3 exposure contributes to the development of type 2 diabetes, particularly among those with higher levels of leisure-time outdoor physical activity. Policies and strategies are needed to reduce O3 exposure to guarantee that the health benefits of physical activity are not diminished by higher levels of O3 pollution in susceptible populations such as older Hispanics. https://doi.org/10.1289/EHP8620.

Metabolic dysfunction modifies the influence of traffic-related air pollution and noise exposure on late-life dementia and cognitive impairment: A cohort study of older Mexican-Americans.

Cognitive impairment has been linked to traffic-related air pollution and noise exposure as well as to metabolic syndrome or some of its individual components. Here, we investigate whether the presence of metabolic dysfunction modifies associations between air pollution or noise exposures and incident dementia or cognitive impairment without dementia (CIND). METHODS: For 1,612 elderly Mexican-American participants of the Sacramento Area Latino Study on Aging (SALSA) followed for up to 10 years, we estimated residential-based local traffic-related exposures relying on the California Line Source Dispersion Model version 4 (CALINE4) for nitrogen oxides (NOx) and the SoundPLAN software package (Version 8.0; NAVCON, Fullerton, CA) that implements the Federal Highway Administration Traffic Noise Model (TNM) for noise, respectively. We used Cox proportional hazard models to estimate the joint effects of NOx or noise exposures and obesity, hyperglycemia, or low high-density lipoprotein (HDL) cholesterol. RESULTS: The risk of developing dementia/CIND among participants with hyperglycemia who also were exposed to high levels of NOx (≥3.44 parts per billion [ppb] [75th percentile]) or noise (≥65 dB) was 2.4 (1.4, 4.0) and 2.2 (1.7, 3.9), respectively. For participants with low HDL-cholesterol, the estimated hazard ratios for dementia/CIND were 2.5 (1.4, 4.3) and 1.8 (1.0, 3.0) for those also exposed to high levels of NOx (≥3.44 ppb) or noise (≥65 dB), respectively, compared with those without metabolic dysfunction exposed to low traffic-related air pollution or noise levels. CONCLUSIONS: Exposure to traffic-related air pollution or noise most strongly increases the risk of dementia/CIND among older Mexican-Americans living in California who also exhibit hyperglycemia or low HDL-cholesterol.

Air pollution, noise exposure, and metabolic syndrome - A cohort study in elderly Mexican-Americans in Sacramento area.

BACKGROUND: Previous studies suggested that air pollutants may increase the incidence of metabolic syndrome, but the potential impact from traffic sources is not well-understood. This study aimed to investigate associations between traffic-related nitrogen oxides (NOx) or noise pollution and risk of incident metabolic syndrome and its components in an elderly Mexican-American population. METHODS: A total of 1,554 Mexican-American participants of the Sacramento Area Latino Study on Aging (SALSA) cohort were followed from 1998 to 2007. We used anthropometric measures and biomarkers to define metabolic syndrome according to the recommendations of the Third Adult Treatment Panel of the National Cholesterol Education Program (NCEP ATP III). Based on participants' residential addresses at baseline, estimates of local traffic-related NOx were generated using the California Line Source Dispersion Model version 4 (CALINE4), and of noise employing the SoundPLAN software package. We used Cox regression models with calendar time as the underlying time scale to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for associations of air pollution or noise with metabolic syndrome or its components. RESULTS: Each per unit increase of traffic-related NOx (2.29 parts per billion (ppb)) was associated with a 15% (HR = 1.15, 95% CI: 1.04-1.28) lower level of high-density lipoprotein cholesterol (HDL-cholesterol), and each 11.6 decibels (dB) increase in noise increased the risk of developing metabolic syndrome by 17% (HR = 1.17, 95% CI: 1.01-1.35). CONCLUSION: Policies aiming to reduce traffic-related air pollution and noise might mitigate the risk of metabolic syndrome and its components in vulnerable populations.

Traffic-related Noise Exposure and Late-life Dementia and Cognitive Impairment in Mexican-Americans.

BACKGROUND: Recently, it has been suggested that environmental exposures from traffic sources including noise may play a role in cognitive impairment in the elderly. The objective of the study was to investigate the association between local traffic-related noise pollution and incident dementia or cognitive impairment without dementia (CIND) during a 10-year follow-up period. METHODS: 1612 Mexican-American participants from the Sacramento Area Latino Study on Aging (SALSA) were followed every 12-15 months via home visits from 1998 to 2007. We used the SoundPLAN software package to estimate noise originating from local traffic with the input of Annual Average Daily Traffic (AADT) data from Metropolitan Planning Organizations (MPO) based on geocoded residential addresses at baseline (1998-1999). We estimated the risks of incident dementia or CIND from 24-hour and nighttime noise exposure using Cox proportional hazard models. RESULTS: During the follow-up, we identified 159 incident dementia or CIND cases in total. Per 11.6 dB (interquartile range width) increase in 24-hour noise, the hazard of developing dementia or CIND increased (hazard ratio = 1.3 [1.0, 1.6]) during follow-up; estimates were slightly lower (hazard ratio = 1.2 [0.97, 1.6]) when adjusting for modeled local air pollution exposure from traffic sources. Overall, the risk of dementia/CIND was elevated when 24-hour and nighttime noise were higher than 75 and 65 dB respectively. See video Abstract: http://links.lww.com/EDE/B728. CONCLUSIONS: In our study, traffic-related noise exposure was associated with increased risk of dementia or CIND in elderly Mexican-Americans. Future studies taking into account other noise sources and occupational noise exposure before retirement are needed.

Long-Term Ozone Exposure and Mortality in a Large Prospective Study.

RATIONALE: Tropospheric ozone (O3) is potentially associated with cardiovascular disease risk and premature death. Results from long-term epidemiological studies on O3 are scarce and inconclusive. OBJECTIVES: In this study, we examined associations between chronic ambient O3 exposure and all-cause and cause-specific mortality in a large cohort of U.S. adults. METHODS: Cancer Prevention Study II participants were enrolled in 1982. A total of 669,046 participants were analyzed, among whom 237,201 deaths occurred through 2004. We obtained estimates of O3 concentrations at the participant's residence from a hierarchical Bayesian space-time model. Estimates of fine particulate matter (particulate matter with an aerodynamic diameter of up to 2.5 µm [PM2.5]) and NO2 concentrations were obtained from land use regression. Cox proportional hazards regression models were used to examine mortality associations adjusted for individual- and ecological-level covariates. MEASUREMENTS AND MAIN RESULTS: In single-pollutant models, we observed significant positive associations between O3, PM2.5, and NO2 concentrations and all-cause and cause-specific mortality. In two-pollutant models adjusted for PM2.5, significant positive associations remained between O3 and all-cause (hazard ratio [HR] per 10 ppb, 1.02; 95% confidence interval [CI], 1.01-1.04), circulatory (HR, 1.03; 95% CI, 1.01-1.05), and respiratory mortality (HR, 1.12; 95% CI, 1.08-1.16) that were unchanged with further adjustment for NO2. We also observed positive mortality associations with both PM2.5 (both near source and regional) and NO2 in multipollutant models. CONCLUSIONS: Findings derived from this large-scale prospective study suggest that long-term ambient O3 contributes to risk of respiratory and circulatory mortality. Substantial health and environmental benefits may be achieved by implementing further measures aimed at controlling O3 concentrations.