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Late-life ambient air pollution is a risk factor for brain aging, but it remains unknown if improved air quality (AQ) lowers dementia risk. We studied a geographically diverse cohort of older women dementia free at baseline in 2008 to 2012 (n = 2,239, aged 74 to 92). Incident dementia was centrally adjudicated annually. Yearly mean concentrations of fine particulate matter (PM2.5) and nitrogen dioxide (NO2) were estimated using regionalized national universal kriging models and averaged over the 3-y period before baseline (recent exposure) and 10 y earlier (remote exposure). Reduction from remote to recent exposures was used as the indicator of improved AQ. Cox proportional hazard ratios (HRs) for dementia risk associated with AQ measures were estimated, adjusting for sociodemographic, lifestyle, and clinical characteristics. We identified 398 dementia cases during follow up (median = 6.1 y). PM2.5 and NO2 reduced significantly over the 10 y before baseline. Larger AQ improvement was associated with reduced dementia risks (HRPM2.5 0.80 per 1.78 µg/m3, 95% CI 0.71-0.91; HRNO2 0.80 per 3.91 parts per billion, 95% CI 0.71-0.90), equivalent to the lower risk observed in women 2.4 y younger at baseline. Higher PM2.5 at baseline was associated with higher dementia risk (HRPM2.5 1.16 per 2.90 µg/m3, 95% CI 0.98-1.38), but the lower dementia risk associated with improved AQ remained after further adjusting for recent exposure. The observed associations did not substantially differ by age, education, geographic region, Apolipoprotein E e4 genotypes, or cardiovascular risk factors. Long-term AQ improvement in late life was associated with lower dementia risk in older women.
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Poluição do Ar/análise , Demência/epidemiologia , Idoso , Idoso de 80 Anos ou mais , Poluentes Atmosféricos/análise , Estudos de Coortes , Exposição Ambiental/efeitos adversos , Feminino , Humanos , Incidência , Dióxido de Nitrogênio , Material Particulado/análise , Modelos de Riscos Proporcionais , Fatores de RiscoRESUMO
The methodological development of this article is motivated by the need to address the following scientific question: does the issuance of heat alerts prevent adverse health effects? Our goal is to address this question within a causal inference framework in the context of time series data. A key challenge is that causal inference methods require the overlap assumption to hold: each unit (i.e., a day) must have a positive probability of receiving the treatment (i.e., issuing a heat alert on that day). In our motivating example, the overlap assumption is often violated: the probability of issuing a heat alert on a cooler day is near zero. To overcome this challenge, we propose a stochastic intervention for time series data which is implemented via an incremental time-varying propensity score (ItvPS). The ItvPS intervention is executed by multiplying the probability of issuing a heat alert on day $t$-conditional on past information up to day $t$-by an odds ratio $\delta_t$. First, we introduce a new class of causal estimands, which relies on the ItvPS intervention. We provide theoretical results to show that these causal estimands can be identified and estimated under a weaker version of the overlap assumption. Second, we propose nonparametric estimators based on the ItvPS and derive an upper bound for the variances of these estimators. Third, we extend this framework to multisite time series using a spatial meta-analysis approach. Fourth, we show that the proposed estimators perform well in terms of bias and root mean squared error via simulations. Finally, we apply our proposed approach to estimate the causal effects of increasing the probability of issuing heat alerts on each warm-season day in reducing deaths and hospitalizations among Medicare enrollees in 2837 US counties.
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Temperatura Alta , Medicare , Idoso , Humanos , Estados Unidos , Fatores de Tempo , Pontuação de Propensão , HospitalizaçãoRESUMO
BACKGROUND: Extreme ambient heat is unambiguously associated with higher risk of illness and death. The Optum Labs Data Warehouse (OLDW), a database of medical claims from US-based patients with commercial or Medicare Advantage health insurance, has been used to quantify heat-related health impacts. Whether results for the insured sub-population are generalizable to the broader population has to our knowledge not been documented. We sought to address this question, for the US population in California from 2012 to 2019. METHODS: We examined changes in daily rates of emergency department (ED) encounters and in-patient hospitalization encounters for all-causes, heat-related outcomes, renal disease, mental/behavioral disorders, cardiovascular disease, and respiratory disease. OLDW was the source for health data for insured individuals in California, and health data for the broader population were gathered from the California Department of Health Care Access and Information (HCAI). We defined extreme heat exposure as any day in a group of 2 or more days with maximum temperatures exceeding the county-specific 97.5 th percentile and used a space-time-stratified case-crossover design to assess and compare the impacts of heat on health. RESULTS: Average incidence rates of medical encounters differed by dataset. However, rate ratios for ED encounters were similar across datasets for all causes (ratio of incidence rate ratios (rIRR) = 0.989; 95% confidence interval (CI) = 0.973, 1.011), heat-related causes (rIRR = 1.080; 95% CI = 0.999, 1.168), renal disease (rIRR = 0.963; 95% CI = 0.718, 1.292), and mental health disorders (rIRR = 1.098; 95% CI = 1.004, 1.201). Rate ratios for inpatient encounters were also similar. CONCLUSIONS: This work presents evidence that OLDW can continue to be a resource for estimating the health impacts of extreme heat.
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BACKGROUND: Few epidemiologic studies have examined the association of ambient heat with spontaneous abortion, a common and devastating pregnancy outcome. METHODS: We conducted a case-crossover study nested within Pregnancy Study Online, a preconception cohort study (2013-2022). We included all participants reporting spontaneous abortion (n=1,524). We defined the case window as the 7 days preceding the event and used time-stratified referent selection to select control windows matched on calendar month and day of week. Within each 7-day case and control window, we measured mean, maximum, and minimum of daily maximum outdoor air temperatures. We fit splines to examine non-linear relationships across the entire year and conditional logistic regression to estimate odds ratios (OR) and 95% CI of spontaneous abortion with increases in temperature during the warm season (May-September) and decreases during the cool season (November-March). RESULTS: We found evidence of a U-shaped association between outdoor air temperature and spontaneous abortion risk based on year-round data. When restricting to warm season events (n=657), the OR for a 10-percentile increase in the mean of lag 0-6 daily maximum temperatures was 1.1 (95% CI: 0.96, 1.2) and, for the maximum, 1.1 (95% CI: 0.99, 1.2). The OR associated with any extreme heat days (>95th county-specific percentile) in the preceding week was 1.2 (95% CI: 0.95, 1.5). Among cool season events (n=615), there was no appreciable association between lower temperatures and spontaneous abortion risk. CONCLUSION: Our study provides evidence of an association between high outdoor temperatures and incidence of spontaneous abortion.
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BACKGROUND: Tropical cyclones are associated with acute increases in mortality and morbidity, but few studies have examined their longer-term health consequences. We assessed whether tropical cyclones are associated with a higher frequency of symptom exacerbation among children with asthma in the following 12 months in eastern United States counties, 2000-2018. METHODS: We defined exposure to tropical cyclones as a maximum sustained windspeed >21 meters/second at the county center and used coarsened exact matching to match each exposed county to one or more unexposed counties. We used longitudinal, de-identified administrative claims data to estimate the county-level, monthly risk of experiencing at least one asthma exacerbation requiring medical attention among commercially insured children aged 5-17 with prior diagnosis of asthma. We used a difference-in-differences approach implemented via a Poisson fixed effects model to compare the risk of asthma exacerbation in the 12 months before versus after each storm in exposed versus unexposed counties. RESULTS: Across 43 tropical cyclones impacting the eastern United States, we did not observe evidence of an increase in the risk of symptom exacerbation in the 12 months following the storm (random-effects meta-analytic summary estimate: risk ratio = 1.03 [95% confidence interval = 0.96, 1.10], I2 = 17%). However, certain storms, such as Hurricane Sandy, were associated with a higher risk of symptom exacerbation. CONCLUSIONS: These findings are consistent with the hypothesis that some tropical cyclones are detrimental to children's respiratory health. However, tropical cyclones were not associated in aggregate with long-term exacerbation of clinically apparent asthma symptoms among a population of children with commercial health insurance.
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Asma , Tempestades Ciclônicas , Criança , Humanos , Exacerbação dos Sintomas , Asma/epidemiologia , Saúde da Criança , Progressão da DoençaRESUMO
Cross-sectional studies-often defined as those in which exposure and outcome are assessed at the same point in time-are frequently viewed as minimally informative for causal inference. While cross-sectional studies may be susceptible to reverse causality, may be limited to assessment of disease prevalence rather than incidence, or may only provide estimates of current rather than past exposures, not all cross-sectional studies suffer these limitations. Moreover, none of these concerns are unique to or inherent in the structure of a cross-sectional study. Regardless of when exposure and disease were ascertained relative to one another, a cross-sectional study may provide insights into the causal effects of exposure on disease incidence. Simply labeling a study as "cross-sectional" and assuming that 1 or more of these limitations exist and are materially important fails to recognize the need for a more nuanced assessment and risks discarding evidence that may be useful in assessing causal relationships.
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Estudos Transversais , Humanos , CausalidadeRESUMO
BACKGROUND: Evidence of associations between daily variation in air pollution and blood pressure (BP) is varied and few prior longitudinal studies adjusted for calendar time. METHODS: We studied 143,658 postmenopausal women 50 to 79 years of age from the Women's Health Initiative (1993-2005). We estimated daily atmospheric particulate matter (PM) (in three size fractions: PM2.5, PM2.5-10, and PM10) and nitrogen dioxide (NO2) concentrations at participants' residential addresses using validated lognormal kriging models. We used linear mixed-effects models to estimate the association between air pollution concentrations and repeated measures of systolic and diastolic BP (SBP, DBP) adjusting for confounders and calendar time. RESULTS: Short-term PM2.5 and NO2 were each positively associated with DBP {0.10 mmHg [95% confidence interval (CI): 0.04, 0.15]; 0.13 mmHg (95% CI: 0.09, 0.18), respectively} for interquartile range changes in lag 3-5 day PM2.5 and NO2. Short-term NO2 was negatively associated with SBP [-0.21 mmHg (95%CI: -0.30, -0.13)]. In two-pollutant models, the NO2-DBP association was slightly stronger, but for PM2.5 was attenuated to null, compared with single-pollutant models. Associations between short-term NO2 and DBP were more pronounced among those with higher body mass index, lower neighborhood socioeconomic position, and diabetes. When long-term (annual) and lag 3-5 day PM2.5 were in the same model, associations with long-term PM2.5 were stronger than for lag 3-5 day. CONCLUSIONS: We observed that short-term PM2.5 and NO2 levels were associated with increased DBP, although two-pollutant model results suggest NO2 was more likely responsible for observed associations. Long-term PM2.5 effects were larger than short-term.
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Poluição do Ar , Poluentes Ambientais , Feminino , Humanos , Idoso , Pressão Sanguínea , Dióxido de Nitrogênio , Poluição do Ar/efeitos adversos , Material ParticuladoRESUMO
Worldwide, millions of people are co-exposed to arsenic and cadmium. Environmental exposure to both metals is linked with a higher risk of atherosclerosis. While studies have characterized the pro-atherosclerotic effects of arsenic and cadmium as single agents, little is known about the potential effects of metal mixtures, particularly at low doses. Here, we used a combination of in vitro and in vivo models to assess the effects of low-dose metals individually and as mixtures on early events and plaque development associated with atherosclerosis. In vitro, we investigated early pro-atherogenic changes in macrophages and endothelial cells with metal treatments. The combined cytotoxic effects of both metals at low concentrations were dose interactive, specifically, synergistic in macrophages, but antagonistic in endothelial cells. Despite this differential behavior across cell types, the mixtures did not initiate early pro-atherogenic events: neither reactive oxygen species generation in macrophages nor adhesion molecule expression on endothelial cells. In vivo, we utilized the well-characterized hyperlipidemic apolipoprotein E knock-out (ApoE-/-) mouse model. Previously, we have shown that low concentrations of arsenic (down to 10 ppb) enhance atherosclerosis in ApoE-/- mice. This model has also been used with cadmium to demonstrate pro-atherogenic effects, although at concentrations above human-relevant exposures. In both sexes, there are some small increases in atherosclerotic lesion size, but very few changes in plaque constituents in the ApoE-/- mouse model. Together, these results suggests that low-dose metal mixtures are not significantly more pro-atherogenic than either metal alone.
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Arsênio , Aterosclerose , Placa Aterosclerótica , Masculino , Feminino , Humanos , Animais , Camundongos , Arsênio/toxicidade , Cádmio/toxicidade , Células Endoteliais/metabolismo , Aterosclerose/metabolismo , Placa Aterosclerótica/induzido quimicamente , Metais , Apolipoproteínas E/genéticaRESUMO
Policy Points After decades of scientific progress and growth in academic literature, there is a recognition that climate change poses a substantial threat to the health and well-being of individuals and communities both in the United States and globally. Solutions to mitigate and adapt to climate change can have important health cobenefits. A vital component of these policy solutions is that they must also take into consideration historic issues of environmental justice and racism, and implementation of these policies must have a strong equity lens.
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Mudança Climática , Humanos , Estados UnidosRESUMO
Objectives. To examine commonalities and gaps in the content of local US heat action plans (HAPs) designed to decrease the adverse health effects of extreme heat. Methods. We used content analysis to identify common strategies and gaps in extreme heat preparedness among written HAPs in the United States from jurisdictions that serve municipalities with more than 200 000 residents. We reviewed, coded, and analyzed plans to assess the prevalence of key components and strategies. Results. All 21 plans evaluated incorporated data on activation triggers, heat health messaging and risk communication, cooling centers, surveillance activities, and agency coordination, and 95% incorporated information on outreach to at-risk populations. Gaps existed in the specific applications of these broad strategies. Conclusions. Practice-based recommendations as well as future areas of research should focus on increasing targeted strategies for at-risk individuals and expanding the use of surveillance data outside of situational awareness. (Am J Public Health. 2023;113(5):559-567. https://doi.org/10.2105/AJPH.2022.307217).
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Calor Extremo , Humanos , Cidades , Comunicação , Temperatura Alta , Fatores de Risco , Estados UnidosRESUMO
Little is known about the combined impact of the COVID-19 pandemic and other major disasters on mental health. Hurricane Harvey hit the Gulf Coast in 2017, resulting in substantial costs, significant levels of displacement, and approximately 100 deaths, and was followed in 2020 by the COVID-19 pandemic. We randomly sampled 1167 Houstonians from 88 designated super-neighborhoods and surveyed them about their demographics, event-specific traumas and stressors, and symptoms of current depression and post-traumatic stress disorder (PTSD). We estimated the prevalence of depression (5.8%) and PTSD (12.6%) more than three years after Hurricane Harvey, and assessed the relative influence of event-specific stressors and traumas on current mental health. Overall, we observed evidence for two key findings that are salient for residents of urban environments in the context of multiple disasters. First, stressors were primary influences on depression, whereas both stressors and traumas influenced PTSD. Second, the influences of stressors and traumas on depression and PTSD symptoms faded with time.
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COVID-19 , Tempestades Ciclônicas , Desastres , Transtornos de Estresse Pós-Traumáticos , Humanos , Transtornos de Estresse Pós-Traumáticos/psicologia , Depressão/epidemiologia , Depressão/psicologia , Pandemias , COVID-19/epidemiologiaRESUMO
BACKGROUND: Ambient particulate matter (PM) air pollution is a leading cause of global disability and accounts for an annual 2.9 million deaths globally. PM is established as an important risk factor for cardiovascular disease, however the evidence supporting a link specifically between long-term exposure to ambient PM and incident stroke is less clear. We sought to evaluate the association of long-term exposure to different size fractions of ambient PM with incident stroke (overall and by etiologic subtypes) and cerebrovascular deaths within the Women's Health Initiative, a large prospective study of older women in the US. METHODS: We studied 155,410 postmenopausal women without previous cerebrovascular disease enrolled into the study between 1993 and 1998, with follow-up through 2010. We assessed geocoded participant address-specific concentrations of ambient PM (fine [PM2.5], respirable [PM10] and coarse [PM10-2.5]), as well as nitrogen dioxide [NO2] using spatiotemporal models. We classified hospitalization events into ischemic, hemorrhagic, or other/unclassified stroke. Cerebrovascular mortality was defined as death from any stroke etiology. We used Cox proportional hazard models to calculate hazard ratios (HR) and 95% confidence intervals (CI), adjusting for individual and neighborhood-level characteristics. RESULTS: During a median follow-up time of 15 years, participants experienced 4,556 cerebrovascular events. The hazard ratio for all cerebrovascular events was 2.14 (95% CI: 1.87, 2.44) comparing the top versus bottom quartiles of PM2.5. Similarly, there was a statistically significant increase in events comparing the top versus bottom quartiles of PM10 and NO2 (HR: 1.17; 95% CI: 1.03, 1.33 and HR:1.26; 95% CI: 1.12, 1.42). The strength of association did not vary substantially by stroke etiology. There was little evidence of an association between PMcoarse and incident cerebrovascular events. CONCLUSIONS: Long-term exposure to fine (PM2.5) and respirable (PM10) particulate matter as well as NO2 was associated with a significant increase of cerebrovascular events among postmenopausal women. Strength of the associations were consistent by stroke etiology.
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Poluentes Atmosféricos , Poluição do Ar , Acidente Vascular Cerebral , Humanos , Feminino , Idoso , Material Particulado/análise , Poluentes Atmosféricos/análise , Estudos Prospectivos , Dióxido de Nitrogênio , Poluição do Ar/análise , Saúde da Mulher , Exposição Ambiental/análiseRESUMO
BACKGROUND: Studies of the association between aircraft noise and hypertension are complicated by inadequate control for potential confounders and a lack of longitudinal assessments, and existing evidence is inconclusive. OBJECTIVES: We evaluated the association between long-term aircraft noise exposure and risk of hypertension among post-menopausal women in the Women's Health Initiative Clinical Trials, an ongoing prospective U.S. METHODS: Day-night average (DNL) and night equivalent sound levels (Lnight) were modeled for 90 U.S. airports from 1995 to 2010 in 5-year intervals using the Aviation Environmental Design Tool and linked to participant geocoded addresses from 1993 to 2010. Participants with modeled exposures ≥45 A-weighted decibels (dB [A]) were considered exposed, and those outside of 45 dB(A) who also did not live in close proximity to unmodeled airports were considered unexposed. Hypertension was defined as systolic/diastolic blood pressure ≥140/90 mmHg or inventoried/self-reported antihypertensive medication use. Using time-varying Cox proportional hazards models, we estimated hazard ratios (HRs) for incident hypertension when exposed to DNL or Lnight ≥45 versus <45 dB(A), controlling for sociodemographic, behavioral, and environmental/contextual factors. RESULTS/DISCUSSION: There were 18,783 participants with non-missing DNL exposure and 14,443 with non-missing Lnight exposure at risk of hypertension. In adjusted models, DNL and Lnight ≥45 db(A) were associated with HRs of 1.00 (95% confidence interval [CI]: 0.93, 1.08) and 1.06 (95%CI: 0.91, 1.24), respectively. There was no evidence supporting a positive exposure-response relationship, and findings were robust in sensitivity analyses. Indications of elevated risk were seen among certain subgroups, such as those living in areas with lower population density (HRinteraction: 0.84; 95%CI: 0.72, 0.98) or nitrogen dioxide concentrations (HRinteraction: 0.82; 95%CI: 0.71, 0.95), which may indicate lower ambient/road traffic noise. Our findings do not suggest a relationship between aircraft noise and incident hypertension among older women in the U.S., though associations in lower ambient noise settings merit further investigation.
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Hipertensão , Ruído dos Transportes , Humanos , Feminino , Idoso , Pós-Menopausa , Estudos Prospectivos , Ruído dos Transportes/efeitos adversos , Hipertensão/epidemiologia , Hipertensão/etiologia , Aeronaves , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análiseRESUMO
BACKGROUND: Increasingly frequent and intense extreme heat events (EHEs) are indicative of climate change impacts, and urban areas' social and built environments increase their risk for health consequences. Heat action plans (HAPs) are a strategy to bolster municipal EHE preparedness. The objective of this research is to characterize municipal interventions to EHEs and compare U.S. jurisdictions with and without formal heat action plans. METHODS: An online survey was sent to 99 U.S. jurisdictions with populations > 200,000 between September 2021 and January 2022. Summary statistics were calculated to describe the proportion of total jurisdictions, as well as jurisdictions with and without HAPs and in different geographies that reported engagement in extreme heat preparedness and response activities. RESULTS: Thirty-eight (38.4%) jurisdictions responded to the survey. Of those respondents, twenty-three (60.5%) reported the development of a HAP, of which 22 (95.7%) reported plans for opening cooling centers. All respondents reported conducting heat-related risk communications; however, communication approaches focused on passive, technology-dependent mechanisms. While 75.7% of jurisdictions reported having developed a definition for an EHE, less than two-thirds of responding jurisdictions reported any of the following activities: conducting heat-related surveillance (61.1%), implementing provisions for power outages (53.1%), increasing access to fans or air conditioners (48.4%), developing heat vulnerability maps (43.2%), or evaluating activities (34.2%). There were only two statistically significant (p ≥ .05) differences in the prevalence of heat-related activities between jurisdictions with and without a written HAP, possibly attributable to a relatively small sample size: surveillance and having a definition of extreme heat. CONCLUSIONS: Jurisdictions can strengthen their extreme heat preparedness by expanding their consideration of at-risk populations to include communities of color, conducting formal evaluations of their responses, and by bridging the gap between the populations determined to be most at-risk and the channels of communication designed to reach them.
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Calor Extremo , Saúde Pública , Humanos , Estados Unidos , Calor Extremo/efeitos adversos , Temperatura Alta , Fatores de Risco , Mudança Climática , Inquéritos e QuestionáriosRESUMO
BACKGROUND: Late-life exposure to ambient air pollution is a modifiable risk factor for dementia, but epidemiological studies have shown inconsistent evidence for cognitive decline. Air quality (AQ) improvement has been associated with improved cardiopulmonary health and decreased mortality, but to the best of our knowledge, no studies have examined the association with cognitive function. We examined whether AQ improvement was associated with slower rate of cognitive decline in older women aged 74 to 92 years. METHODS AND FINDINGS: We studied a cohort of 2,232 women residing in the 48 contiguous US states that were recruited from more than 40 study sites located in 24 states and Washington, DC from the Women's Health Initiative (WHI) Memory Study (WHIMS)-Epidemiology of Cognitive Health Outcomes (WHIMS-ECHO) study. They were predominantly non-Hispanic White women and were dementia free at baseline in 2008 to 2012. Measures of annual (2008 to 2018) cognitive function included the modified Telephone Interview for Cognitive Status (TICSm) and the telephone-based California Verbal Learning Test (CVLT). We used regionalized universal kriging models to estimate annual concentrations (1996 to 2012) of fine particulate matter (PM2.5) and nitrogen dioxide (NO2) at residential locations. Estimates were aggregated to the 3-year average immediately preceding (recent exposure) and 10 years prior to (remote exposure) WHIMS-ECHO enrollment. Individual-level improved AQ was calculated as the reduction from remote to recent exposures. Linear mixed effect models were used to examine the associations between improved AQ and the rates of cognitive declines in TICSm and CVLT trajectories, adjusting for sociodemographic (age; geographic region; race/ethnicity; education; income; and employment), lifestyle (physical activity; smoking; and alcohol), and clinical characteristics (prior hormone use; hormone therapy assignment; depression; cardiovascular disease (CVD); hypercholesterolemia; hypertension; diabetes; and body mass index [BMI]). For both PM2.5 and NO2, AQ improved significantly over the 10 years before WHIMS-ECHO enrollment. During a median of 6.2 (interquartile range [IQR] = 5.0) years of follow-up, declines in both general cognitive status (ß = -0.42/year, 95% CI: -0.44, -0.40) and episodic memory (ß = -0.59/year, 95% CI: -0.64, -0.54) were observed. Greater AQ improvement was associated with slower decline in TICSm (ßPM2.5improvement = 0.026 per year for improved PM2.5 by each IQR = 1.79 µg/m3 reduction, 95% CI: 0.001, 0.05; ßNO2improvement = 0.034 per year for improved NO2 by each IQR = 3.92 parts per billion [ppb] reduction, 95% CI: 0.01, 0.06) and CVLT (ßPM2.5 improvement = 0.070 per year for improved PM2.5 by each IQR = 1.79 µg/m3 reduction, 95% CI: 0.02, 0.12; ßNO2improvement = 0.060 per year for improved NO2 by each IQR = 3.97 ppb reduction, 95% CI: 0.005, 0.12) after adjusting for covariates. The respective associations with TICSm and CVLT were equivalent to the slower decline rate found with 0.9 to 1.2 and1.4 to 1.6 years of younger age and did not significantly differ by age, region, education, Apolipoprotein E (ApoE) e4 genotypes, or cardiovascular risk factors. The main limitations of this study include measurement error in exposure estimates, potential unmeasured confounding, and limited generalizability. CONCLUSIONS: In this study, we found that greater improvement in long-term AQ in late life was associated with slower cognitive declines in older women. This novel observation strengthens the epidemiologic evidence of an association between air pollution and cognitive aging.
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Poluentes Atmosféricos/efeitos adversos , Poluição do Ar/efeitos adversos , Disfunção Cognitiva/epidemiologia , Exposição Ambiental/efeitos adversos , Vida Independente/tendências , Entrevistas como Assunto/métodos , Idoso , Idoso de 80 Anos ou mais , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Disfunção Cognitiva/prevenção & controle , Disfunção Cognitiva/psicologia , Estudos de Coortes , Exposição Ambiental/prevenção & controle , Feminino , Seguimentos , Humanos , Vida Independente/psicologia , Estudos Longitudinais , Material Particulado/efeitos adversos , Material Particulado/análise , Melhoria de Qualidade , Estados Unidos/epidemiologia , Aprendizagem Verbal/fisiologiaRESUMO
BACKGROUND: Epidemiologic studies suggest cadmium exposure is associated with cardiovascular disease risk, including heart failure. However, prior findings may be influenced by tobacco smoking, a dominant source of cadmium exposure and risk factor for heart failure. The present study leverages up to 20 years of follow-up in the Danish Diet, Cancer and Health cohort to examine the relationship between urinary cadmium and incident heart failure among people who never smoked. METHODS: Between 1993 and 1997, 19,394 never-smoking participants (ages 50-64 years) enrolled and provided a urine sample. From this sample, we randomly selected a subcohort of 600 men and 600 women and identified 958 incident heart failure cases occurring between baseline and 2015. Using a case-cohort approach, we estimated adjusted hazard ratios (aHR) for heart failure in Cox proportional hazards models with age as the time scale. RESULTS: Participants had relatively low concentrations of urinary cadmium, as expected for never smokers (median = 0.20; 25th, 75th = 0.13, 0.32 µg cadmium/g creatinine). In adjusted models, we found that higher urinary cadmium was associated with a higher rate of incident heart failure overall (aHR = 1.1 per interquartile range difference [95% CI = 1.0, 1.2). In sex-stratified analyses, the association seemed restricted to men (aHR = 1.5 [95% CI = 1.2, 1.9]). CONCLUSIONS: In this cohort of people who never smoked tobacco, environmental cadmium was positively associated with incident heart failure, especially among men.
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Cádmio , Insuficiência Cardíaca , Cádmio/análise , Estudos de Coortes , Dinamarca/epidemiologia , Exposição Ambiental/análise , Feminino , Insuficiência Cardíaca/epidemiologia , Humanos , Masculino , Pessoa de Meia-Idade , Fatores de Risco , FumantesRESUMO
AIMS: We estimated the association between outdoor light at night at the residence and risk of coronary heart disease (CHD) within a prospective cohort of older adults in Hong Kong. METHODS AND RESULTS: Over a median of 11 years of follow-up, we identified 3772 incident CHD hospitalizations and 1695 CHD deaths. Annual levels of outdoor light at night at participants' residential addresses were estimated using time-varying satellite data for a composite of persistent night-time illumination at â¼1 km2 scale. We used Cox proportional hazards models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) of the association between outdoor light at night at the residence and risk of CHD. The association between light at night and incident CHD hospitalization and mortality exhibited a monotonic exposure-response function. An interquartile range (IQR) (60.0 nW/cm2/sr) increase in outdoor light at night was associated with an HR of 1.11 (95% CI: 1.03, 1.18) for CHD hospitalizations and 1.10 (95% CI: 1.00, 1.22) for CHD deaths after adjusting for both individual and area-level risk factors. The association did not vary across strata of hypothesized risk factors. CONCLUSION: Among older adults, outdoor light at night at the residence was associated with a higher risk of CHD hospitalizations and deaths. We caution against causal interpretation of these novel findings. Future studies with more detailed information on exposure, individual adaptive behaviours, and potential mediators are warranted to further examine the relationship between light at night and CHD risk.
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Doença das Coronárias , Idoso , Estudos de Coortes , Doença das Coronárias/epidemiologia , Doença das Coronárias/etiologia , Hong Kong/epidemiologia , Humanos , Incidência , Modelos de Riscos Proporcionais , Estudos Prospectivos , Fatores de RiscoRESUMO
The magnitude, timing, and etiology of morbidity associated with tropical cyclones remains incompletely quantified. We examined the relative change in cause-specific emergency department (ED) visits among residents of New York City during and after Hurricane Sandy, a tropical cyclone that affected the northeastern United States in October 2012. We used quasi-Poisson constrained distributed lag models to compare the number of ED visits on and after Hurricane Sandy with all other days, 2005-2014, adjusting for temporal trends. Among residents aged ≥65 years, Hurricane Sandy was associated with a higher rate of ED visits due to injuries and poisoning (relative risk (RR) = 1.19, 95% confidence interval (CI): 1.10, 1.28), respiratory disease (RR = 1.35, 95% CI: 1.21, 1.49), cardiovascular disease (RR = 1.10, 95% CI: 1.02, 1.19), renal disease (RR = 1.44, 95% CI: 1.22, 1.72), and skin and soft tissue infections (RR = 1.20, 95% CI: 1.03, 1.39) in the first week following the storm. Among adults aged 18-64 years, Hurricane Sandy was associated with a higher rate of ED visits for renal disease (RR = 2.15, 95% CI: 1.79, 2.59). Among those aged 0-17 years, the storm was associated with lower rates of ED visits for up to 3 weeks. These results suggest that tropical cyclones might result in increased health-care utilization due to a wide range of causes, particularly among older adults.
Assuntos
Tempestades Ciclônicas/estatística & dados numéricos , Desastres/estatística & dados numéricos , Serviço Hospitalar de Emergência/estatística & dados numéricos , Utilização de Instalações e Serviços/estatística & dados numéricos , Adolescente , Adulto , Distribuição por Idade , Idoso , Criança , Pré-Escolar , Tempestades Ciclônicas/história , Desastres/história , Serviço Hospitalar de Emergência/história , Utilização de Instalações e Serviços/história , Feminino , História do Século XXI , Humanos , Lactente , Recém-Nascido , Masculino , Pessoa de Meia-Idade , Cidade de Nova Iorque/epidemiologia , Distribuição de Poisson , Adulto JovemRESUMO
BACKGROUND: A growing body of evidence links maternal exposure to particulate matter <2.5 µM in diameter (PM2.5) and deviations in fetal growth. Several studies suggest that the placenta plays a critical role in conveying the effects of maternal PM2.5 exposure to the developing fetus. These include observed associations between air pollutants and candidate placental features, such as mitochondrial DNA content, DNA methylation and telomere length. However, gaps remain in delineating the pathways linking the placenta to air pollution-related health effects, including a comprehensive profiling of placental processes impacted by maternal PM2.5 exposure. In this study, we examined alterations in a placental transcriptome-wide network in relation to maternal PM2.5 exposure prior to and during pregnancy and infant birthweight. METHODS: We evaluated PM2.5 exposure and placental RNA-sequencing data among study participants enrolled in the Rhode Island Child Health Study (RICHS). Daily residential PM2.5 levels were estimated using a hybrid model incorporating land-use regression and satellite remote sensing data. Distributed lag models were implemented to assess the impact on infant birthweight due to PM2.5 weekly averages ranging from 12 weeks prior to gestation until birth. Correlations were assessed between PM2.5 levels averaged across the identified window of susceptibility and a placental transcriptome-wide gene coexpression network previously generated using the WGCNA R package. RESULTS: We identified a sensitive window spanning 12 weeks prior to and 13 weeks into gestation during which maternal PM2.5 exposure is significantly associated with reduced infant birthweight. Two placental coexpression modules enriched for genes involved in amino acid transport and cellular respiration were correlated with infant birthweight as well as maternal PM2.5 exposure levels averaged across the identified growth restriction window. CONCLUSION: Our findings suggest that maternal PM2.5 exposure may alter placental programming of fetal growth, with potential implications for downstream health effects, including susceptibility to cardiometabolic health outcomes and viral infections.
Assuntos
Poluentes Atmosféricos , Poluição do Ar , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Peso ao Nascer , Criança , Feminino , Redes Reguladoras de Genes , Humanos , Lactente , Exposição Materna/efeitos adversos , Material Particulado/análise , Material Particulado/toxicidade , Placenta/química , Gravidez , Rhode IslandRESUMO
BACKGROUND: and Purpose: Cadmium has been associated with risk of cardiovascular events, including stroke. Human cadmium exposure occurs primarily through diet and tobacco smoke. Recent cohort studies have found an association with stroke, but residual confounding from smoking, could not be ruled out. We therefore conducted a case-cohort study to evaluate whether cadmium is associated with stroke in never-smokers. METHODS: The Danish Diet Cancer and Health cohort consists of Danes 50-64 years old, recruited in 1993-1997. From never-smoking cohort members without previous cancer or stroke we sampled a sub-cohort of 1200 persons. We also identified all (n = 534) cases in the cohort with a validated stroke diagnosis between baseline and 2009. We quantified cadmium and creatinine concentrations from baseline urine samples and used cadmium per creatinine as our main exposure metric. We used Cox proportional hazards models to estimate hazard ratios (HRs) with age as time scale and adjusting for BMI, education and urinary cotinine with and without stratification by sex. RESULTS: The median urinary cadmium concentration was 0.21 µg cadmium/g creatinine in cases and 0.19 µg/g in the sub-cohort. The majority (83%) of stroke cases were diagnosed with ischemic stroke. The HR for stroke in the highest quartile of exposure (median 0.44 µg/g creatinine) was 1.11 (95% CI: 0.79-1.54) compared with the lowest quartile (median 0.10 µg/g creatinine). The HR per inter quartile range (IQR, 0.19 µg/g creatinine) was 1.02 (95% CI: 0.92-1.12). Among men, the HR per IQR higher levels of cadmium (0.16 µg/g creatinine) was 1.18 (95% CI: 0.92-1.52), and 1.00 (95% CI: 0.89-1.12) among women. Adjusting for creatinine or using osmolality instead of creatinine standardization generally attenuated observed relationships. CONCLUSIONS: Our results do not support that low levels of cadmium exposure among never-smokers are strongly associated with risk of stroke, although results varied somewhat by sex and method of accounting for urinary dilution.