UCLA

Cognitive impairment is a major concern for older adults especially in societies with increasing life expectancy and aging populations, since it reduces health related quality of life and increases caregiver burden. Possible and established factors for cognitive impairment not only include age, genetics, race/ethnicity, life style factors, but also metabolic syndrome, and evidence is accumulating that links environmental risk factors to cognitive impairment such as air pollution and noise exposure. As one of the risk factors of cognitive impairment, metabolic syndrome (MetS) refers to a collection of reversible pathophysiologic conditions including insulin resistance, obesity, dyslipidemia and hypertension. It is highly prevalent in the Hispanic population especially among those aged 60 years or older. In this dissertation, our aim was to investigate the influence of exposures to traffic-related air pollution and noise on incident metabolic syndrome and cognitive impairment, and whether the presence of metabolic syndrome would modify the association between air pollution or noise exposure and cognitive decline in elderly Mexican-Americans.

The following studies used data from the Sacramento Area Latino Study on Aging (SALSA), a prospective cohort study of 1789 Mexican-Americans aged 60-101, who were living in the Sacramento Area of California between 1998 and 2007. Based on participants’ residential addresses at baseline, we estimated local traffic-related nitrogen oxides (NOx) exposure using the California Line Source Dispersion Model version 4 (CALINE4), and traffic noise employing the SoundPLAN software package.

For 1,554 SALSA participants who were free of all five components of MetS at baseline according to the recommendations of the Third Adult Treatment Panel of the National

Cholesterol Education Program (NCEP ATP III), we investigated associations between modeled traffic-related NOx or noise pollution and incident metabolic syndrome or its components using Cox regression models with calendar time as the underlying time scale. We found that per unit increase in traffic-related NOx (2.29 parts per billion (ppb)) the hazard ratio (HR) for having low level of high-density lipoprotein cholesterol (HDL-cholesterol) increased by 15% (HR=1.15, 95% CI: 1.04–1.28), and for each 11.6 decibels (dB) increase in noise the risk of developing metabolic syndrome increased by 17% (HR=1.17, 95% CI: 1.01–1.35).

Some epidemiological studies started to focus on associations between air pollution and cognitive function recently, while the role of traffic noise in relation to cognitive impairment is under-studied. Here, we examined association between traffic-related noise pollution and dementia/ cognitive impairment without dementia (CIND) that developed newly over a 10-year follow-up period among 1,612 participants who were free of dementia/CIND at enrollment. Using Cox proportional hazard models, we observed that per 11.6dB (interquartile range, IQR) increase in 24-hour noise, the hazard of developing dementia/CIND increased (HR = 1.24, 95% CI: 1.00, 1.53) during follow-up; estimates were slightly lower (HR = 1.19, 95% CI: 0.95, 1.49) 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 75dB and 65dB, respectively.

In the third study, we investigated whether the presence of metabolic dysfunction (obesity, hyperglycemia and low HDL-cholesterol) modifies associations between air pollution or noise exposures and incident dementia or CIND. Among the 1,612 participants from SALSA study who were cognitively normal at the baseline, we used Cox proportional hazard models with calendar time as the underlying time scale to estimate the joint effects of air pollution and noise exposures and several metabolic dysfunctions, specially obesity, hyperglycemia, or low HDL-cholesterol. We found that the risk of developing dementia/CIND increased most (more than 2-fold) among SALSA participants who were exposed to high levels of traffic-related NOx (≥ 3.44 ppb [75th percentile]) (HR = 2.36, 95% CI = 1.41, 3.97) or 24-hour noise (≥ 65 dB) (HR = 2.21, 95% CI = 1.26, 3.89), respectively, and had hyperglycemia. The estimated hazard ratios for dementia/CIND were similarly increased with traffic related air pollution or noise exposures among participants with low HDL-cholesterol but no difference were seen for obesity.

Employing data from one of the large population-based studies of Mexican-Americans, in which repeated anthropometric measurements and sampling of biomarkers as well as repeated cognitive function testing, we added for the linkage between traffic-related air pollution and noise exposures with metabolic syndrome and cognitive impairment. We additionally improve the understanding for the role that metabolic dysfunctions play in the association between traffic-related exposures and cognitive decline. Early identification and treatment of people with metabolic dysfunction as well as prevention approaches that restricting the traffic-related exposures in residential neighborhoods might provide an effective avenue to generate public health benefits in vulnerable populations of elderly.