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BACKGROUND: Air pollutants may contribute to the development of Parkinson's disease (PD), but empirical evidence is limited and inconsistent. OBJECTIVES: This study aimed to prospectively investigate the associations of PD with ambient exposures to fine particulate matter with aerodynamic diameter = 2.5μm (PM2.5) and nitrogen dioxide (NO2). METHODS: We analyzed data from 47,108 US women from the Sister Study, enrolled from 2003–2009 (35–80 years of age) and followed through 2018. Exposures of interest included address-level ambient PM2.5 and NO2 in 2009 and their cumulative averages from 2009 to PD diagnosis with varying lag-years. The primary outcome was PD diagnosis between 2009 and 2018 (푛 = 163). We used multivariable Cox proportional hazards and time-varying Cox models to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). RESULTS: NO2 exposure in 2009 was associated with PD risk in a dose-response manner. The HR and 95% CI were 1.22 (95% CI: 1.03, 1.46) for one interquartile [4.8 parts per billion (ppb)] increment in NO2, adjusting for age, race and ethnicity, education, smoking status, alcohol drinking, caffeine intake, body mass index, physical activity, census region, residential area type, area deprivation index (ADI), and self-reported health status. The association was confirmed in secondary analyses with time-varying averaged cumulative exposures. For example, the multivariable adjusted HR for PD per 4.8 ppb increment in NO2 was 1.25 (95% CI: 1.05, 1.50) in the 2-year lag analysis using cumulative average exposure. Post hoc subgroup analyses overall confirmed the association. However, statistical interaction analyses found that the positive association of NO2 with PD risk was limited to women in urban, rural, and small town areas and women with = 50th percentile ADI but not among women from suburban areas or areas with < 50th percentile ADI. In contrast, PM2.5 exposure was not associated with PD risk with the possible exception for women from the Midwest region of the US (HRinterquartile-range = 2.49, 95% CI: 1.20, 5.14) but not in other census regions. DISCUSSION: In this nationwide cohort of US women, higher level exposure to ambient NO2 is associated with a greater risk of PD. This finding needs to be independently confirmed and the underlying mechanisms warrant further investigation. [ABSTRACT FROM AUTHOR]

Objectives Recent meta-analyses suggest a physical activity health paradox: high levels of occupational physical activity (OPA) increase cardiovascular disease (CVD) risk, while leisure-time physical activity (LTPA) decreases risk. However, studies of women and cerebrovascular disease are limited. This report examines physical activity effects on stroke and transient ischemic attack (TIA) among working women in the United States. Methods OPA history, health status, and lifestyle were assessed by baseline interviews of 31 270 employed Sister Study participants aged 35-74 years. OPA was assessed at six intensity levels (lowest: "mostly sitting"); the highest three were combined as "high intensity work." Independent OPA and LTPA effects on 6-year cerebrovascular disease incidence were estimated in adjusted Cox proportional hazard models. Results Stroke (N=441) and TIA (N=274) risk increased with more standing and higher intensity work at current and longest held job. Compared with mostly sitting, high intensity work at the current job increased TIA risk by 57% [hazard ratio (HR) 1.57, 95% confidence interval (CI) 1.04-2.38]. High intensity OPA at the longest held job increased risk for stroke by 44% (HR 1.44; 95% CI 1.08-1.93). Among women with CVD, sitting and standing equally, especially at the current job, increased risks up to two-fold (TIA HR 1.98, 95% CI 1.10-3.55) compared with mostly sitting at work. LTPA showed inverse associations. Conclusions Higher intensity levels of OPA increased stroke and TIA risks, while LTPA decreased risks; results corroborate the physical activity health paradox for women and cerebrovascular disease. More standing at work increased cerebrovascular disease risks, especially for women with CVD. [ABSTRACT FROM AUTHOR]

BACKGROUND: Olfactory impairment (OI) is common among older adults and independently predicts all-cause mortality and the risk of several major neurodegenerative diseases. Pesticide exposure may impair olfaction, but empirical evidence is lacking. OBJECTIVE: We aimed to examine high pesticide exposure events (HPEEs) in relation to self-reported OI in participants in the Agricultural Health Study (AHS). METHODS: We conducted multivariable logistic regression to examine the associations between HPEEs reported at enrollment (1993-1997) and self-reported OI at the latest AHS follow-up (2013-2015) among 11,232 farmers, using farmers without HPEEs as the reference or unexposed group. RESULTS: A total of 1,186 (10.6%) farmers reported OI. A history of HPEEs reported at enrollment was associated with a higher likelihood of reporting OI two decades later {odds ratio ðORÞ=1:49 [95% confidence interval (CI): 1.28, 1.73]}. In the analyses on the HPEE involving the highest exposure, the association appears to be stronger when there was a >4-h delay between HPEE and washing with soap and water [e.g., OR=2:07 (95% CI: 1.48, 2.89) for 4-6 h vs. OR=1:39 (95% CI: 1.11, 1.75) for <30 min]. Further, significant associations were observed both for HPEEs involving the respiratory or digestive tract [OR=1:53 (95% CI: 1.22, 1.92)] and dermal contact [OR=1:47 (95% CI: 1.22, 1.78)]. Finally, we found significant associations with several specific pesticides involved in the highest exposed HPEEs, including two organochlorine insecticides (DDT and lindane) and four herbicides (alachlor, metolachlor, 2,4-D, and pendimethalin). HPEEs that occurred after enrollment were also associated with OI development. CONCLUSIONS: HPEEs may cause long-lasting olfactory deficit. Future studies should confirm these findings with objectively assessed OI and also investigate potential mechanisms. [ABSTRACT FROM AUTHOR]

Background: Olfactory impairment is common among older adults; however, data are largely limited to whites.Methods: We conducted pooled analyses of two community-based studies: the Atherosclerosis Risk in Communities study (ARIC, 1,398 blacks and 4,665 whites), and the Health, Aging, and Body Composition study (Health ABC, 958 blacks and 1,536 whites) to determine the prevalence of anosmia and associated factors for black and white older adults in the United States.Results: The overall prevalence of anosmia was 22.3% among blacks and 10.4% among whites. Blacks had a markedly higher odds of anosmia compared to whites in age and sex adjusted analyses (odds ratio [OR] 2.96, 95% confidence interval [CI] = 2.59-3.38). In both blacks and whites, higher anosmia prevalence was associated with older age and male sex. The highest prevalence was found in black men 85 years or older (58.3%), and the lowest in white women aged 65-69 years (2.4%). Higher education level, lower cognitive score, ApoE ε4, daytime sleepiness, poorer general health status, lower body mass index, and Parkinson disease were associated with higher prevalence of anosmia in one or both races. However, the racial difference in anosmia remained statistically significant after adjusting for these factors (fully adjusted OR = 1.76, 95%CI: 1.50-2.07). Results were comparable between the two cohorts.Discussion: Anosmia is common in older adults, particularly among blacks. Further studies are needed to identify risk factors for anosmia and to investigate racial disparities in this sensory deficit. [ABSTRACT FROM AUTHOR]

BACKGROUND: Age-related macular degeneration (AMD) is a leading cause of blindness in developed countries. Few studies have investigated its relationship to environmental neurotoxicants. In previous cross-sectional studies, we found an association between pesticide use and self-reported retinal degeneration. OBJECTIVE: We evaluated the association of pesticide use with physician-confirmed incident AMD. METHODS: The Agricultural Health Study (AHS) is a prospective cohort of pesticide applicators and their spouses enrolled from 1993-1997 in Iowa and North Carolina. Cohort members reported lifetime use of 50 specific pesticides at enrollment. Self-reports of incident AMD during follow-up through 2007 were confirmed by reports from participants' physicians and by independent evaluation of retinal photographs provided by the physicians. Confirmed cases (n=161) were compared with AHS cohort members without AMD (n=39,108). We estimated odds ratios (ORs) and 95% confidence intervals (CIs) by logistic regression with adjustment for age, gender, and smoking. RESULTS: AMD was associated with ever use of organochlorine [OR=2:7 (95% CI: 1:8, 4:0)] and organophosphate [OR =2:0 (95% CI: 1.3, 3.0)] insecticides and phenoxyacetate herbicides [OR=1:9 (95% CI: 1:2, 2:8)]. Specific pesticides consistently associated with AMD included chlordane, dichlorodiphenyltrichloroethane (DDT), malathion, and captan; others with notable but slightly less consistent associations were heptachlor, diazinon, phorate, 2,4,5-trichlorophenoxyacetic acid (2,4,5-T), and 2,4-dichlorophenoxyacetic acid (2,4-D). Results were similar for men and women. Some specific pesticides were associated with both early- and late-stage AMD, but others were associated with only one stage. CONCLUSIONS: Exposures to specific pesticides may be modifiable risk factors for AMD. [ABSTRACT FROM AUTHOR]

Background: Several studies suggest that cancer is reduced before and after a Parkinson's disease (PD) diagnosis. However, determining relationships among diseases of ageing is challenging due to possible biases in ascertaining disease. This study evaluates the PD and cancer relationship, addressing potential biases.Methods: Using Surveillance, Epidemiology, and End Results-Medicare linked data (1992-2005) of adults ≥ 65 years, we assessed PD risk after cancer comparing PD in 743 779 cancer patients with PD in a non-cancer group (n = 419 432) in prospective cohort analyses. We also conducted a case-control study of 836 947 cancer cases and 142 869 controls to assess cancer following PD. We applied Cox proportional hazards models to estimate hazards ratios (HRs) for PD after cancer and unconditional logistic regression to estimate odds ratios (ORs) for PD preceding cancer, controlling for physician visits and other factors. To explore biases in ascertaining cancer, we examined relationships between cancer and automobile accident injuries, which we expected to be null.Results: No association was observed between cancer and subsequent PD [HR = 0.97; 95% confidence interval (CI) = 0.92-1.01] nor between cancer and subsequent automobile injuries (HR = 1.03; 95% CI = 0.98-1.07). One site, lung cancer, was associated with subsequent reduced PD, which may reflect confounding by smoking. In the case-control analysis, PD was associated with reduced subsequent cancer, overall (OR = 0.77; 95% CI = 0.71-0.82) and for several cancer sites. However, the automobile injury/ subsequent cancer association was similar (OR = 0.83; 95% CI = 0.78-0.88), suggesting a cancer detection bias after serious health outcomes.Conclusions: In totality, our data do not support a biological relationship between PD and cancer. [ABSTRACT FROM AUTHOR]

OBJECTIVE--To investigate the relationship between diabetes and future risk of Parkinson's disease (PD) among older U.S. adults. RESEARCH DESIGN AND METHODS--A prospective study of self-reported diabetes in 1995 and 1996 in relation to PD diagnosed after 1995 among 288,662 participants of the National Institutes of Health-AARP Diet and Health Study. Multivariate odds ratio (OR) and 95% CI were derived from logistic regression models. RESULTS--A total of 1,565 participants with PD diagnosed after 1995 were included in the analysis. After adjustment for potential confounders, PD risk was ~40% higher (OR = 1.41 [95% CI 1.20-1.66]) among diabetic patients than among participants without diabetes. Further analysis showed that the risk elevation was largely limited to individuals who had diabetes for more than 10 years at the time of baseline survey (1.75 [1.36-2.25]). The association with diabetes was seen for both participants with PD diagnosed between 1995 and 1999 and participants with PD diagnosed after 2000. In addition, similar results were obtained after excluding participants with stroke, heart disease, cancers, or poor or fair health status and in subgroup analyses by age, sex, smoking status, and coffee consumption. CONCLUSIONS--This large study showed that diabetes was associated with a higher future risk of PD and the nature of this association warrants further investigation. [ABSTRACT FROM AUTHOR]

OBJECTIVES: To investigate whether indicators of obesity are associated with functional disabilities in elderly American women and men. DESIGN: Cross-sectional. SETTING: National Health and Nutrition Examination Survey (NHANES) 1999 to 2004, United States. PARTICIPANTS: One thousand six hundred eighty-four elderly (aged ≥60) women and 1,611 elderly men. MEASUREMENTS: Functional disabilities. RESULTS: In women, body mass index (BMI) and waist circumference were each related to higher prevalence of all measures of disabilities. Compared with the lowest quartile of waist circumference, the multivariate odds ratios (ORs) of the highest quartile for having difficulties in functional domains were 2.4 (95% confidence interval (CI)=1.6–3.6) for activities of daily living, 2.3 (95% CI=1.6–3.3) for instrumental activities of daily living, 2.6 (95% CI=1.6–4.1) for leisure and social activities, 4.8 (95% CI=3.4–6.9) for lower extremity mobility, and 2.9 (95% CI=2.1–4.0) for general physical activity. In men, these associations were moderate; the corresponding ORs were 1.2 (95% CI=0.8–2.0), 1.3 (95% CI=0.9–2.1), 2.1 (95% CI=1.2–3.7), 1.8 (95% CI=1.2–2.7), and 2.1 (95% CI=1.5–2.8), respectively. Similar results were obtained for BMI. These associations could not be explained by the presence of major chronic conditions. When adjusted simultaneously, waist circumference appeared to be a better predictor than BMI of disability in women. CONCLUSION: The results suggest that indicators of obesity are related to functional disabilities in elderly Americans. [ABSTRACT FROM AUTHOR]

Dietary iron is the most important source of iron stores. Several case-control studies have described the association of high dietary iron and Parkinsons disease, but prospective data are lacking. The authors prospectively followed 47,406 men and 76,947 women from the United States who provided information through a mailed questionnaire on their diet, medical history, and lifestyle practices between 1984 and 2000. The authors documented 422 new cases of Parkinsons disease. Total iron intake was not associated with an increased risk of Parkinsons disease (relative risk (RR) = 1.10, 95% confidence interval (CI): 0.74, 1.65; Ptrend = 0.84), but dietary nonheme iron intake from food was associated with a 30% increased risk of Parkinsons disease (RR = 1.27, 95% CI: 0.92, 1.76; Ptrend = 0.02). A secondary analysis revealed that Parkinsons disease risk was significantly increased among individuals with high nonheme iron and low vitamin C intakes (RR = 1.92, 95% CI: 1.14, 3.32; Ptrend = 0.002). Supplemental iron intake was associated with a borderline increase in Parkinsons disease risk among men. Although the authors’ prospective data did not support an association between total iron intake (dietary and supplemental) and risk of Parkinsons disease, a 30% increased risk was associated with a diet rich in nonheme iron. This increase in risk was present in those who had low vitamin C intake. [ABSTRACT FROM AUTHOR]