Search

Background: The potential for residential greenness to improve cardiovascular health through both physical and psychological mechanisms is well recognized. However, evidence from rapidly urbanizing developing countries and cohort-based causal inference approaches, remains limited. We aim to examine the effect of residential greenness and time to cardiovascular mortality in South China. Methods: We utilized data from a community-based population survey involving 748,209 participants at baseline from 2009 to 2015, followed up until 2020. Residential greenness exposure was assessed by the annual Normalized Difference Vegetation Index (NDVI) in the 500 m radius of each participant’s residence. We used time-varying proportional hazard Cox models coupled with inverse probability weighting to fit marginal structural models and obtain hazard ratios (HRs) for cardiovascular disease (CVD) mortality after adjusting for confounders. Multiple effect modifiers on both additive and multiplicative scales were further explored. Results: A total of 15,139 CVD-related deaths were identified during a median of 7.9 years of follow-up. A protective effect was found between higher greenness exposure and reduced CVD mortality, with a 9.3 % lower rate of total CVD mortality (HR 0.907, 95 % CI 0.859–0.957) based on a 0.1 increase in annual average NDVI. Demographic (age, marital status) and lifestyle factors (smoking, drinking status) were found to modify the association between residential greenness and CVD mortality (all P interaction values

Background Epidemiological findings regarding the association of particulate matter [less than or equal to]2.5 [mu]m (PM.sub.2.5) exposure with hypertensive disorders in pregnancy (HDP) are inconsistent; evidence for HDP risk related to PM.sub.2.5 components, mixture effects, and windows of susceptibility is limited. We aimed to investigate the relationships between HDP and exposure to PM.sub.2.5 during pregnancy. Methods and findings A large retrospective cohort study was conducted among mothers with singleton pregnancies in Kaiser Permanente Southern California from 2008 to 2017. HDP were defined by International Classification of Diseases-9/10 (ICD-9/10) diagnostic codes and were classified into 2 subcategories based on the severity of HDP: gestational hypertension (GH) and preeclampsia and eclampsia (PE-E). Monthly averages of PM.sub.2.5 total mass and its constituents (i.e., sulfate, nitrate, ammonium, organic matter, and black carbon) were estimated using outputs from a fine-resolution geoscience-derived model. Multilevel Cox proportional hazard models were used to fit single-pollutant models; quantile g-computation approach was applied to estimate the joint effect of PM.sub.2.5 constituents. The distributed lag model was applied to estimate the association between monthly exposure and HDP risk. This study included 386,361 participants (30.3 ± 6.1 years) with 4.8% (17,977/373,905) GH and 5.0% (19,381/386,361) PE-E cases, respectively. In single-pollutant models, we observed increased relative risks for PE-E associated with exposures to PM.sub.2.5 total mass [adjusted hazard ratio (HR) per interquartile range: 1.07, 95% confidence interval (CI) [1.04, 1.10] p < 0.001], black carbon [HR = 1.12 (95% CI [1.08, 1.16] p < 0.001)] and organic matter [HR = 1.06 (95% CI [1.03, 1.09] p < 0.001)], but not for GH. The population attributable fraction for PE-E corresponding to the standards of the US Environmental Protection Agency (9 [mu]g/m.sup.3) was 6.37%. In multi-pollutant models, the PM.sub.2.5 mixture was associated with an increased relative risk of PE-E ([HR = 1.05 (95% CI [1.03, 1.07] p < 0.001)], simultaneous increase in PM.sub.2.5 constituents of interest by a quartile) and PM.sub.2.5 black carbon gave the greatest contribution of the overall mixture effects (71%) among all individual constituents. The susceptible window is the late first trimester and second trimester. Furthermore, the risks of PE-E associated with PM.sub.2.5 exposure were significantly higher among Hispanic and African American mothers and mothers who live in low- to middle-income neighborhoods (p < 0.05 for Cochran's Q test). Study limitations include potential exposure misclassification solely based on residential outdoor air pollution, misclassification of disease status defined by ICD codes, the date of diagnosis not reflecting the actual time of onset, and lack of information on potential covariates and unmeasured factors for HDP. Conclusions Our findings add to the literature on associations between air pollution exposure and HDP. To our knowledge, this is the first study reporting that specific air pollution components, mixture effects, and susceptible windows of PM.sub.2.5 may affect GH and PE-E differently., Author(s): Yi Sun 1,2, Rashmi Bhuyan 2,3,4, Anqi Jiao 2, Chantal C. Avila 5, Vicki Y. Chiu 5, Jeff M. Slezak 5, David A. Sacks 5,6, John Molitor 7, Tarik [...]

Background Numerous studies have linked fine particulate matter (PM2.5) to increased cardiovascular mortality. Less is known how the PM2.5-cardiovascular mortality association varies by use of cardiovascular medications. This study sought to quantify effect modification by statin use status on the associations between long-term exposure to PM2.5 and mortality from any cardiovascular cause, coronary heart disease (CHD), and stroke. Methods In this nested case-control study, we followed 1.2 million community-dwelling adults aged ≥66 years who lived in Ontario, Canada from 2000 through 2018. Cases were patients who died from the three causes. Each case was individually matched to up to 30 randomly selected controls using incidence density sampling. Conditional logistic regression models were used to estimate odds ratios (ORs) for the associations between PM2.5 and mortality. We evaluated the presence of effect modification considering both multiplicative (ratio of ORs) and additive scales (the relative excess risk due to interaction, RERI). Results Exposure to PM2.5 increased the risks for cardiovascular, CHD, and stroke mortality. For all three causes of death, compared with statin users, stronger PM2.5-mortality associations were observed among non-users [e.g. for cardiovascular mortality corresponding to each interquartile range increase in PM2.5, OR = 1.042 (95% CI, 1.032–1.053) vs OR = 1.009 (95% CI, 0.996–1.022) in users, ratio of ORs = 1.033 (95% CI, 1.019–1.047), RERI = 0.039 (95% CI, 0.025–0.050)]. Among users, partially adherent users exhibited a higher risk of PM2.5-associated mortality than fully adherent users. Conclusions The associations of chronic exposure to PM2.5 with cardiovascular and CHD mortality were stronger among statin non-users compared to users. [ABSTRACT FROM AUTHOR]

Introduction In the United States, a 2020 study found that ~5,600 annual excess deaths across the country were attributable to heat, which is substantially higher than previously reported. (1) Marginalized [...]

Background: As atmospheric greenhouse gas concentrations continue to rise, temperature and humidity will increase further, causing potentially dire increases in human heat stress. On physiological and biophysical grounds, exposure to higher levels of humidity should worsen heat stress by decreasing sweat evaporation. However, population-scale epidemiological studies of heat exposure and response often do not detect associations between high levels of humidity and heat-related mortality or morbidity. These divergent, disciplinary views regarding the role of humidity in heat-related health risks limit confidence in selecting which interventions are effective in reducing health impacts and in projecting future heat-related health risks. Objectives: Via our multidisciplinary perspective we seek to a) reconcile the competing realities concerning the role of humidity in heat-related health impacts and b) help ensure robust projections of heat-related health risks with climate change. These objectives are critical pathways to identify and communicate effective approaches to cope with present and future heat challenges. Discussion: We hypothesize six key reasons epidemiological studies have found little impact of humidity on heat- health outcomes: a) At high temperatures, there may be limited influence of humidity on the health conditions that cause most heat-related deaths (i.e., cardiovascular collapse); b) epidemiological data sets have limited spatial extent, a bias toward extratropical (i.e., cooler and less humid), high-income nations, and tend to exist in places where temporal variations in temperature and humidity are positively correlated; c) analyses focus on older, vulnerable populations with sweating, and thus evaporative, impairments that may be further aggravated by dehydration; d) extremely high levels of temperature and humidity (seldom seen in the historical record) are necessary for humidity to substantially impact heat strain of sedentary individuals; e) relationships between temperature and humidity are improperly considered when interpreting epidemiological model results; and f) sub-daily meteorological phenomena, such as rain, occur at high temperatures and humidity, and may bias epidemiological studies based on daily data. Future research must robustly test these hypotheses to advance methods for more accurate incorporation of humidity in estimating heat-related health outcomes under present and projected future climates. https://doi.org/10.1289/EHP11807, Introduction Heat extremes have dire consequences for human health, increasing mortality, morbidity, and occupational health hazards. Heat-health risks are heightened for people who are older, (1,2) have chronic diseases, (3,4) [...]

BACKGROUND: Numerous epidemiological studies have documented the adverse health impact of long-term exposure to fine particulate matter [particulate matter [less than or equal to]2.5 [micro]m in aerodynamic diameter (P[M.sub.2.5])] on mortality even at relatively low levels. However, methodological challenges remain to consider potential regulatory intervention's complexity and provide actionable evidence on the predicted benefits of interventions. We propose the parametric g-computation as an alternative analytical approach to such challenges. METHOD: We applied the parametric g-computation to estimate the cumulative risks of nonaccidental death under different hypothetical intervention strategies targeting long-term exposure to P[M.sub.2.5] in the Canadian Community Health Survey cohort from 2005 to 2015. On both relative and absolute scales, we explored the benefits of hypothetical intervention strategies compared with the natural course that a) set the simulated exposure value at each follow-up year to a threshold value if exposure was above the threshold (8.8 [micro]g/[m.sup.3], 7.04 [micro]g/[m.sup.3], 5 [micro]g/[m.sup.3], and 4 [micro]g/[m.sup.3]), and b) reduced the simulated exposure value by a percentage (5% and 10%) at each follow-up year. We used the 3-y average P[M.sub.2.5] concentration with 1-y lag at the postal code of respondents' annual mailing addresses as their long-term exposure to P[M.sub.2.5]. We considered baseline and time-varying confounders, including demographics, behavior characteristics, income level, and neighborhood socioeconomic status. We also included the R syntax for reproducibility and replication. RESULTS: All hypothetical intervention strategies explored led to lower 11-y cumulative mortality risks than the estimated value under the natural course without intervention, with the smallest reduction of 0.20 per 1,000 participants (95% CI: 0.06, 0.34) under the threshold of 8.8 [micro]g/[m.sup.3], and the largest reduction of 3.40 per 1,000 participants (95% CI: -0.23, 7.03) under the relative reduction of 10% per interval. The reductions in cumulative risk, or numbers of deaths that would have been prevented if the intervention was employed instead of maintaining the status quo, increased over time but flattened toward the end of the follow-up period. Estimates among those [greater than or equal to]65 years of age were greater with a similar pattern. Our estimates were robust to different model specifications. DISCUSSION: We found evidence that any intervention further reducing the long-term exposure to P[M.sub.2.5] would reduce the cumulative mortality risk, with greater benefits in the older population, even in a population already exposed to low levels of ambient P[M.sub.2.5]. The parametric g-computation used in this study provides flexibilities in simulating real-world interventions, accommodates time-varying exposure and confounders, and estimates adjusted survival curves with clearer interpretation and more information than a single hazard ratio, making it a valuable analytical alternative in air pollution epidemiological research. https://doi.org/10.1289/EHP11095, Introduction Given that collective efforts in previous decades have successfully reduced the level of fine particulate matter [particulate matter First, evidence suggested that the risk associated with the changes in [...]

Background Globally, access to life-saving vaccines has improved considerably in the past 5 decades. However, progress has started to slow down and even reverse in recent years. Understanding subnational heterogeneities in essential child immunization will be critical for closing the global vaccination gap. Methods and findings We use vaccination information for over 220,000 children across 1,366 administrative regions in 43 low- and middle-income countries (LMICs) from the most recent Demographic and Health Surveys. We estimate essential immunization coverage at the national and subnational levels and quantify socioeconomic inequalities in such coverage using adjusted concentration indices. Within- and between-country variations are summarized via the Theil index. We use local indicator of spatial association (LISA) statistics to identify clusters of administrative regions with high or low values. Finally, we estimate the number of missed vaccinations among children aged 15 to 35 months across all 43 countries and the types of vaccines most often missed. We show that national-level vaccination rates can conceal wide subnational heterogeneities. Large gaps in child immunization are found across West and Central Africa and in South Asia, particularly in regions of Angola, Chad, Nigeria, Guinea, and Afghanistan, where less than 10% of children are fully immunized. Furthermore, children living in these countries consistently lack all 4 basic vaccines included in the WHO's recommended schedule for young children. Across most countries, children from poorer households are less likely to be fully immunized. The main limitations include subnational estimates based on large administrative divisions for some countries and different periods of survey data collection. Conclusions The identified heterogeneities in essential childhood immunization, especially given that some regions consistently are underserved for all basic vaccines, can be used to inform the design and implementation of localized intervention programs aimed at eliminating child suffering and deaths from existing and novel vaccine-preventable diseases., Author(s): Anna Dimitrova 1,*, Gabriel Carrasco-Escobar 1,2, Robin Richardson 3,4, Tarik Benmarhnia 1 Introduction Vaccination is one of the most cost-effective interventions in public health [1,2] that has led to [...]