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1.
J Epidemiol Community Health ; 64(1): 68-74, 2010 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-19833604

RESUMO

BACKGROUND: Observational studies and controlled experiments have provided evidence that airborne particulate matter (PM) is capable of acutely increasing blood pressure (BP) in certain scenarios. The goal of this study was to evaluate whether and to what extent obesity and community location affect relationships between fine particulate matter (PM(2.5)) and blood pressure (BP) measures. METHODS: Using data from a stratified random sample survey of adults conducted in 2002-3 in Detroit, Michigan, we tested body mass index (BMI) and waist circumference (WCIR) in separate models as effect modifiers of the relationship between PM(2.5) exposure and BP. We also tested interactions with community location. Models were adjusted for covariates with established pro-hypertensive effects. RESULTS: PM(2.5) exposure was positively associated with increased pulse pressure (PP) for those categorised as obese (BMI> or =30) across lags 2 (beta 4.16, p<0.05) and 3 days (beta 2.55, p<0.05) prior to BP measure. WCIR similarly modified the effect of exposure to PM(2.5) on PP (beta 4.34, p<0.003). The observed effects were enhanced in the community with closer proximity to local emissions of PM(2.5), and for residents classified as obese (BMI> or =30) or with WCIR above high-risk cuts points. CONCLUSIONS: This community-based study suggests that positive associations between PM(2.5) exposure and PP and systolic BP are enhanced in areas proximate to sources of PM (2.5) emissions. These patterns were observed for all residents, but were more visible and consistent among those who were obese. Research is needed to examine the mechanistic pathways by which air particles interact with obesity and location to affect BP, and inform community interventions to reduce the population burden of hypertension and related co-morbidities.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Pressão Sanguínea/efeitos dos fármacos , Obesidade/fisiopatologia , Material Particulado/efeitos adversos , Adulto , Índice de Massa Corporal , Coleta de Dados , Feminino , Humanos , Masculino , Michigan , Pessoa de Meia-Idade , Saúde da População Urbana
2.
J Epidemiol Community Health ; 62(7): 638-46, 2008 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-18559448

RESUMO

BACKGROUND: The study was designed to provide evidence of a cascade effect linking socioeconomic position to anthropometric indicators of cardiovascular disease (CVD) risk through effects on psychosocial stress, psychological distress and health-related behaviours, and consider implications for disease prevention and health promotion. METHODS: A cross-sectional stratified two-stage probability sample of occupied housing units in three areas of Detroit, Michigan, was used in the study. 919 adults aged > or =25 years completed the survey (mean age 46.3; 53% annual household income <$20 000; 57% non-Hispanic black, 22% Latino, 19% non-Hispanic white). Variables included self-report (eg, psychosocial stress, depressive symptoms, health behaviours) and anthropometric measurements (eg, waist circumference, height, weight). The main outcome variables were depressive symptoms, smoking status, physical activity, body mass index and waist circumference. RESULTS: Income was inversely associated with depressive symptoms, likelihood of current smoking, physical inactivity and waist circumference. These relationships were partly or fully mediated by psychosocial stress. A suppressor effect of current smoking on the relationship between depressive symptoms and waist circumference was found. Independent effects of psychosocial stress and psychological distress on current smoking and waist circumference were found, above and beyond the mediated pathways. CONCLUSIONS: The results suggest that relatively modest improvements in the income of economically disadvantaged people can set in motion a cascade of effects, simultaneously reducing exposure to stressful life conditions, improving mental well-being, increasing health-promoting behaviours and reducing anthropometric risks associated with CVD. Such interventions offer important opportunities to improve population health and reduce health disparities.


Assuntos
Doenças Cardiovasculares/epidemiologia , Transtorno Depressivo/epidemiologia , Comportamentos Relacionados com a Saúde , Estresse Psicológico/epidemiologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Estatura , Índice de Massa Corporal , Peso Corporal , Estudos Transversais , Etnicidade , Feminino , Humanos , Masculino , Michigan/epidemiologia , Pessoa de Meia-Idade , Atividade Motora , Fatores de Risco , Fumar/epidemiologia , Meio Social , Fatores Socioeconômicos , Saúde da População Urbana , Circunferência da Cintura
3.
Occup Environ Med ; 65(8): 534-40, 2008 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-18032533

RESUMO

OBJECTIVES: Understanding mechanistic pathways linking airborne particle exposure to cardiovascular health is important for causal inference and setting environmental standards. We evaluated whether urinary albumin excretion, a subclinical marker of microvascular function which predicts cardiovascular events, was associated with ambient particle exposure. METHODS: Urinary albumin and creatinine were measured among members of the Multi-Ethnic Study of Atherosclerosis at three visits during 2000-2004. Exposure to PM(2.5) and PM(10) (microg/m(3)) was estimated from ambient monitors for 1 month, 2 months and two decades before visit one. We regressed recent and chronic (20 year) particulate matter (PM) exposure on urinary albumin/creatinine ratio (UACR, mg/g) and microalbuminuria at first examination, controlling for age, race/ethnicity, sex, smoking, second-hand smoke exposure, body mass index and dietary protein (n = 3901). We also evaluated UACR changes and development of microalbuminuria between the first, and second and third visits which took place at 1.5- to 2-year intervals in relation to chronic PM exposure prior to baseline using mixed models. RESULTS: Chronic and recent particle exposures were not associated with current UACR or microalbuminuria (per 10 microg/m(3) increment of chronic PM(10) exposure, mean difference in log UACR = -0.02 (95% CI -0.07 to 0.03) and relative probability of having microalbuminuria = 0.92 (95% CI 0.77 to 1.08)) We found only weak evidence that albuminuria was accelerated among those chronically exposed to particles: each 10 microg/m(3) increment in chronic PM(10) exposure was associated with a 1.14 relative probability of developing microalbuminuria over 3-4 years, although 95% confidence intervals included the null (95% CI 0.96 to 1.36). CONCLUSIONS: UACR is not a strong mechanistic marker for the possible influence of air pollution on cardiovascular health in this sample.


Assuntos
Poluição do Ar/estatística & dados numéricos , Albuminúria/epidemiologia , Exposição por Inalação/estatística & dados numéricos , Material Particulado/toxicidade , Adulto , Idoso , Idoso de 80 Anos ou mais , Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Doenças Cardiovasculares/etnologia , Doenças Cardiovasculares/etiologia , Creatinina/urina , Feminino , Humanos , Exposição por Inalação/efeitos adversos , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Grupos Raciais , Estados Unidos/epidemiologia
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