Age at menarche, reproductive years, and menopause status were significantly associated with body composition, insulin sensitivity and blood lipid levels.

Rationale: Few studies have examined associations between longterm exposure to fine particulate matter (PM 2.5 ) and lung function decline in adults.Objectives: To determine if exposure to traffic and PM 2.5 is associated with longitudinal changes in lung function in a population-based cohort in the Northeastern United States, where pollution levels are relatively low.Methods: FEV 1 and FVC were measured up to two times between 1995 and 2011 among 6,339 participants of the Framingham Offspring or Third Generation studies. We tested associations between residential proximity to a major roadway and PM 2.5 exposure in 2001 (estimated by a land-use model using satellite measurements of aerosol optical thickness) and lung function. We examined differences in average lung function using mixed-effects models and differences in lung function decline using linear regression models. Current smokers were excluded. Models were adjusted for age, sex, height, weight, pack-years, socioeconomic status indicators, cohort, time, season, and weather.Measurements and Main Results: Living less than 100 m from a major roadway was associated with a 23.2 ml (95% confidence interval [CI], 244.4 to 21.9) lower FEV 1 and a 5.0 ml/yr (95% CI, 29.0 to 20.9) faster decline in FEV 1 compared with more than 400 m. Each 2 mg/m 3 increase in average of PM 2.5 was associated with a 13.5 ml (95% CI, 226.6 to 20.3) lower FEV 1 and a 2.1 ml/yr (95% CI, 24.1 to 20.2) faster decline in FEV 1 . There were similar associations with FVC. Associations with FEV 1 /FVC ratio were weak or absent.Conclusions: Long-term exposure to traffic and PM 2.5 , at relatively low levels, was associated with lower FEV 1 and FVC and an accelerated rate of lung function decline.

Background and Purpose Long-term exposure to ambient air pollution is associated with cerebrovascular disease and cognitive impairment, but whether it is related to structural changes in the brain is not clear. We examined the associations between residential long-term exposure to ambient air pollution and markers of brain aging using magnetic resonance imaging (MRI). Methods Framingham Offspring Study participants who attended the seventh examination, were at least 60 years old and free of dementia and stroke were included. We evaluated associations between exposures (fine particulate matter (PM2.5) and residential proximity to major roadways) and measures of total cerebral brain volume, hippocampal volume, white matter hyperintensity volume (log-transformed and extensive white matter hyperintensity volume for age) and covert brain infarcts. Models were adjusted for age, clinical covariates, indicators of socioeconomic position, and temporal trends. Results A 2 μg/m3 increase in PM2.5 was associated with -0.32% (95%CI: -0.59, -0.05) smaller total cerebral brain volume and 1.46 (95%CI: 1.10, 1.94) higher odds of covert brain infarcts. Living further away from a major roadway was associated with 0.10 (95%CI: 0.01, 0.19) greater log-transformed white matter hyperintensity volume for an interquartile range difference in distance, but no clear pattern of association was observed for extensive white matter. Conclusions Exposure to elevated levels of PM2.5 was associated with smaller total cerebral brain volume, a marker of age-associated brain atrophy, and with higher odds of covert brain infarcts. These findings suggest that air pollution is associated with insidious effects on structural brain aging even in dementia-and stroke-free persons.

Background Individually, heart failure (HF) and Alzheimer Disease (AD) are severe threats to population health, and their potential coexistence is an alarming prospect. In addition to sharing analogous epidemiological and genetic profiles, biochemical characteristics, and common triggers, we recently recognized common molecular and pathological features between the 2 conditions. Whereas cognitive impairment has been linked to HF through perfusion defects, angiopathy, and inflammation, whether patients with AD present with myocardial dysfunction, and if the 2 conditions bear a common pathogenesis as neglected siblings is unknown. Objectives Here we investigated if amyloid beta (Aβ) protein aggregates are present in the hearts of patients with a primary diagnosis of AD, affecting myocardial function. Methods We examined myocardial function in a retrospective cross-sectional study from a cohort of AD patients and age-matched controls. Imaging and proteomics approaches were used to identify and quantify Aβ deposits in AD heart and brain specimens compared to controls. Cell shortening and calcium transients were measured on isolated adult cardiomyocytes. Results Echocardiographic measurements of myocardial function suggest that patients with AD present with an anticipated diastolic dysfunction. As in the brain, Aβ40 and Aβ42 are present in the heart, and their expression is increased in AD. Conclusions Here we provide the first report of the presence of compromised myocardial function and intramyocardial deposits of Aβ in AD patients. Our findings depict a novel biological framework in which AD may be viewed either as a systemic disease or as a metastatic disorder leading to heart, and possibly multiorgan failure. AD and HF are both debilitating and life-threatening conditions, affecting enormous patient populations. Our findings underline a previously dismissed problem of a magnitude that will require new diagnostic approaches and treatments for brain and heart disease, and their combination.