Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 8 de 8
Filtrar
Mais filtros











Base de dados
Intervalo de ano de publicação
1.
Environ Int ; 173: 107810, 2023 03.
Artigo em Inglês | MEDLINE | ID: mdl-36870315

RESUMO

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.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Demência , Ruído dos Transportes , Humanos , Idoso , Americanos Mexicanos , Dióxido de Nitrogênio/análise , Exposição Ambiental/efeitos adversos , Estudos de Coortes , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise , Material Particulado/efeitos adversos , Material Particulado/análise , Cognição
2.
Environ Health Perspect ; 129(9): 97004, 2021 09.
Artigo em Inglês | MEDLINE | ID: mdl-34494856

RESUMO

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.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Diabetes Mellitus Tipo 2 , Ozônio , Idoso , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Diabetes Mellitus Tipo 2/epidemiologia , Exposição Ambiental/análise , Exercício Físico , Humanos , Americanos Mexicanos , Ozônio/análise , Material Particulado/análise
3.
Am J Epidemiol ; 189(10): 1124-1133, 2020 10 01.
Artigo em Inglês | MEDLINE | ID: mdl-32383448

RESUMO

Low physical activity (PA) among older adults increases the risk of cardiovascular disease (CVD) and mortality through metabolic disorders such as type 2 diabetes. We aimed to elucidate the extent to which diabetes mediates the effect of nonoccupational PA levels on CVD and mortality among older Mexican Americans. This study included 1,676 adults from the Sacramento Area Latino Study on Aging (1998-2007). We employed Cox proportional hazards regression models to investigate associations of PA level with all-cause mortality, fatal CVD, and nonfatal CVD events. Utilizing causal mediation analysis within a counterfactual framework, we decomposed the total effect of PA into natural indirect and direct effects. Over a median of 8 years of follow-up, low PA (<25th percentile) was associated with increased risks of all-cause mortality (hazard ratio (HR) = 1.36, 95% confidence interval (CI): 1.06, 1.75), fatal CVD (HR = 2.05, 95% CI: 1.42, 2.97), and nonfatal CVD events (HR = 1.67, 95% CI: 1.18, 2.37) in comparison with high PA (>75th percentile). Diabetes mediated 11.0%, 7.4%, and 5.2% of the total effect of PA on all-cause mortality, fatal CVD, and nonfatal CVD events, respectively. Our findings indicate that public health interventions targeting diabetes prevention and management would be a worthwhile strategy for preventing CVD and mortality among older Mexican Americans with insufficient PA levels.


Assuntos
Doenças Cardiovasculares/epidemiologia , Diabetes Mellitus Tipo 2/complicações , Exercício Físico , Americanos Mexicanos/estatística & dados numéricos , Mortalidade , Idoso , California/epidemiologia , Diabetes Mellitus Tipo 2/epidemiologia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade
4.
Environ Int ; 134: 105269, 2020 01.
Artigo em Inglês | MEDLINE | ID: mdl-31778933

RESUMO

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.


Assuntos
Poluição do Ar , Idoso , Poluentes Atmosféricos , Estudos de Coortes , Exposição Ambiental , Feminino , Humanos , Masculino , Síndrome Metabólica , Americanos Mexicanos , Pessoa de Meia-Idade , Ruído , Material Particulado , Emissões de Veículos
5.
Environ Epidemiol ; 4(6): e122, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-33778355

RESUMO

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.

6.
Epidemiology ; 31(6): 771-778, 2020 11 01.
Artigo em Inglês | MEDLINE | ID: mdl-33555809

RESUMO

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.


Assuntos
Disfunção Cognitiva , Demência , Americanos Mexicanos , Ruído dos Transportes , Idoso , Disfunção Cognitiva/etnologia , Demência/etnologia , Humanos , Ruído dos Transportes/efeitos adversos
7.
Am J Epidemiol ; 188(11): 1944-1952, 2019 11 01.
Artigo em Inglês | MEDLINE | ID: mdl-31497846

RESUMO

A higher level of physical activity (PA) is associated with decreased risk of mortality, dementia, and depression, yet the mechanisms involved are not well understood, and little evidence exists for Mexican Americans. With data from the Sacramento Area Latino Study on Aging (1998-2007), we used Cox proportional hazards regression to separately evaluate associations of baseline PA level with mortality, dementia/cognitive impairment without dementia (CIND), and depressive symptoms, and we estimated the mediating effects of inflammatory markers in additive hazard models. A low level of PA (<35 metabolic equivalent of task-hours/week) was associated with increased mortality (hazard ratio (HR) = 1.50, 95% confidence interval (CI): 1.20, 1.88), dementia/CIND (HR = 1.37, 95% CI: 0.96, 1.96), and depressive symptoms (HR = 1.23, 95% CI: 1.00, 1.52). A low PA level added 512 (95% CI: -34, 1,058) cases of dementia/CIND per 100,000 person-years at risk (direct effect), while, through a mediating path, interleukin 6 (IL-6) added another 49 (95% CI: 5, 94) cases, or 9% of the total effect. For mortality, 8%-10% of the PA total effect was mediated through IL-6, tumor necrosis factor α (TNF-α), or TNF-α receptors. None of the inflammatory markers mediated the association between PA and depressive symptoms. Our results suggest that antiinflammation (especially as assessed by IL-6 and TNF-α levels) may partly explain how PA protects against dementia/CIND and mortality.


Assuntos
Demência/epidemiologia , Depressão/epidemiologia , Exercício Físico/psicologia , Inflamação/psicologia , Americanos Mexicanos/estatística & dados numéricos , Mortalidade , Idoso , Biomarcadores/sangue , Proteína C-Reativa/metabolismo , California/epidemiologia , Cognição , Estudos de Coortes , Demência/sangue , Demência/prevenção & controle , Depressão/sangue , Depressão/prevenção & controle , Feminino , Humanos , Inflamação/sangue , Inflamação/epidemiologia , Interleucina-6/sangue , Masculino , Americanos Mexicanos/psicologia , Pessoa de Meia-Idade , Fator de Necrose Tumoral alfa/sangue
8.
Alzheimers Dement ; 14(1): 1-9, 2018 01.
Artigo em Inglês | MEDLINE | ID: mdl-28692819

RESUMO

INTRODUCTION: The etiologies of dementia are complex and influenced by genetic and environmental factors including medical conditions. METHODS: We used Cox regression model to estimate the individual and joint effects of physical activity (PA), apolipoprotein E (APOE) ε4, and diabetes status on risk of dementia and cognitive impairment without dementia (CIND) among 1438 cognitively intact Mexican American elderly who were followed up to 10 years. RESULTS: The risk of developing dementia/CIND was increased more than threefold in APOE ε4 carriers or diabetics with low levels of PA compared with ε4 noncarriers or nondiabetics who engaged in high PA (ε4: hazard ratio [HR] = 3.44, 95% confidence interval [CI] = 1.85-6.39; diabetes: HR = 3.11, 95% CI = 1.87-5.18); the presence of all three risk factors increased risk by nearly 10-fold (HR = 9.49, 95% CI = 3.57-25.3). DISCUSSION: PA in elderly Hispanics protects strongly against the onset of dementia/CIND, especially in APOE ε4 carriers and those who have diabetes.


Assuntos
Envelhecimento , Apolipoproteína E4/genética , Disfunção Cognitiva/etiologia , Demência/etiologia , Diabetes Mellitus Tipo 2/complicações , Exercício Físico/fisiologia , Idoso , Idoso de 80 Anos ou mais , Diabetes Mellitus Tipo 2/genética , Jejum/sangue , Feminino , Predisposição Genética para Doença , Genótipo , Humanos , Estudos Longitudinais , Masculino , Entrevista Psiquiátrica Padronizada , Americanos Mexicanos , Pessoa de Meia-Idade , Testes Neuropsicológicos , Modelos de Riscos Proporcionais , Fatores de Risco
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA