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BackgroundRecently, 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.Methods1612 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.ResultsDuring 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.ConclusionsIn 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.

Most prior work in quantitative approaches to generalizability and transportability emphasizes extending causal effect estimates from randomized trials to target populations. Extending findings from observational studies is also of scientific interest, and identifiability assumptions and estimation methods differ from randomized settings when there is selection on both the exposure and exposure--outcome mediators in combination with exposure--outcome confounders (and both confounders and mediators can modify exposure--outcome effects). We argue that this causal structure is common in observational studies, particularly in the field of life course epidemiology, for example, when extending estimates of the effect of an early-life exposure on a later-life outcome from a cohort enrolled in midlife or late life. We describe identifiability assumptions and identification using observed data in such settings, highlighting differences from work extending findings from randomized trials. We describe statistical methods, including weighting, outcome modeling, and doubly robust approaches, to estimate potential outcome means and average treatment effects in the target population and illustrate performance of the methods in a simulation study. We show that in the presence of selection into the study sample on both exposure and confounders, estimators must be able to address confounding in the target population. When there is also selection on mediators of the exposure--outcome relationship, estimators need to be able to use different sets of variables to account for selection (including the mediator), and confounding. We discuss conceptual implications of our results as well as highlight unresolved practical questions for applied work to extend findings from observational studies to target populations. [ABSTRACT FROM AUTHOR]

BackgroundIn middle age, stroke incidence is higher among black than white Americans. For unknown reasons, this inequality decreases and reverses with age. We conducted simulations to evaluate whether selective survival could account for observed age patterning of black-white stroke inequalities.MethodsWe simulated birth cohorts of 20,000 blacks and 20,000 whites with survival distributions based on US life tables for the 1919-1921 birth cohort. We generated stroke incidence rates for ages 45-94 years using Reasons for Geographic and Racial Disparities in Stroke (REGARDS) study rates for whites and setting the effect of black race on stroke to incidence rate difference (IRD) = 20/10,000 person-years at all ages, the inequality observed at younger ages in REGARDS. We compared observed age-specific stroke incidence across scenarios, varying effects of U, representing unobserved factors influencing mortality and stroke risk.ResultsDespite a constant adverse effect of black race on stroke risk, the observed black-white inequality in stroke incidence attenuated at older age. When the hazard ratio for U on stroke was 1.5 for both blacks and whites, but U only directly influenced mortality for blacks (hazard ratio for U on mortality =1.5 for blacks; 1.0 for whites), stroke incidence rates in late life were lower among blacks (average observed IRD = -43/10,000 person-years at ages 85-94 years versus causal IRD = 20/10,000 person-years) and mirrored patterns observed in REGARDS.ConclusionsA relatively moderate unmeasured common cause of stroke and survival could fully account for observed age attenuation of racial inequalities in stroke.