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The present study introduces a concentration estimation model for indoor inhalable fine particles (PM2.5) during cooking activities in typical Kazakh houses, which are generally poorly ventilated with high emission levels. The aim of the present work is to identify factors influencing PM2.5 concentrations during cooking and elucidate the mechanisms underlying the build‐up and reduction of PM2.5 concentrations. These are achieved through a methodology that combines PM2.5 sampling, monitoring, and modeling to predict household PM2.5 levels and estimate daily concentrations. Specifically, USEPA's IAQX v1.1 was employed to simulate the one‐zone concept (kitchen) for concentrations related to cooking activities in several households. The results reveal that PM2.5 concentrations varied between 13 and 266 μg/m3 during cooking activities. Factors such as kitchen size, air exchange characteristics, and the type of food and cooking style were identified as important, influencing the observed concentrations. The model accurately captured concentration trends (R > 0.9). However, certain predictions tended to overestimate the measurements, attributing to inaccuracies in selecting air exchange and emission rates. Cooking activities contributed to household air pollutant (HAP) PM2.5 levels ranging from 9% to 94%. Notably, during the non‐heating period of the year (corresponding to the warmer half of the year), the impact of cooking became more significant and was identified as a major contributor to indoor PM2.5 concentrations. Conversely, during the heating period (i.e., the colder part of the year), outdoor PM levels and household ventilation practices played primary roles in regulating indoor air concentrations. This present study presents one of the initial efforts to assess household air pollutants in Central Asia, providing foundation and insights into the indoor air quality of Kazakh houses, where the understanding of indoor air quality remains limited. Future research recommendations include developing advanced models that account for individual activity patterns and specific house types for improved accuracy and representativeness. [ABSTRACT FROM AUTHOR]

BackgroundAmong women aged 50 to 59 years at baseline in the Women's Health Initiative (WHI) Estrogen-Alone (E-Alone) trial, randomization to conjugated equine estrogen-alone versus placebo was associated with lower risk of myocardial infarction and mortality, and, in an ancillary study, the WHI-CACS (WHI Coronary Artery Calcification Study) with lower CAC, measured by cardiac computed tomography ≈8.7 years after baseline randomization. We hypothesized that higher CAC would be related to post-trial coronary heart disease (CHD), cardiovascular disease (CVD), and total mortality, independent of baseline randomization or risk factors.Methods and resultsWHI-CACS participants (n=1020) were followed ≈8 years from computed tomography scan in 2005 (mean age=64.4) through 2013 for incident CHD (myocardial infarction and fatal CHD, n=17), CVD (n=69), and total mortality (n=55). Incident CHD and CVD analyses excluded women with CVD before scan (n=89). Women with CAC=0 (n=54%) had very low age-adjusted rates/1000 person-years of CHD (0.91), CVD (5.56), and mortality (3.45). In comparison, rates were ≈2-fold higher for women with any CAC (>0). Associations were not modified by baseline randomization to conjugated equine estrogen-alone versus placebo. Adjusted for baseline randomization and risk factors, the hazard ratio (95% confidence interval) for CAC >100 (19%) was 4.06 (2.11, 7.80) for CVD and 2.70 (1.26, 5.79) for mortality.ConclusionsAmong a subset of postmenopausal women aged 50 to 59 years at baseline in the WHI E-Alone Trial, CAC at mean age of 64 years was strongly related to incident CHD, CVD, and to total mortality over ≈8 years, independent of baseline randomization to conjugated equine estrogen-alone versus placebo or CVD risk factors.Clinical trial registrationURL: https://www.clinicaltrials.gov. Unique identifier: NCT00000611.

Background: The menopausal transition (MT) poses an increased risk for major depression (MD), but not for all women. Current and past stress are toxic risk factors for depression throughout life. The MT may be a time of increased sensitivity to stress, especially among women with a lifetime history of major depressive disorder (MDD). We evaluated whether women who experienced childhood maltreatment (CM) or current stressful events or ongoing problems were at increased risk for MD during the MT. Methods: At the Pittsburgh site of the Study of Women's Health Across the Nation, 333 midlife women were interviewed approximately annually over 15 years with the Structured Clinical Interview for the Diagnosis of DSM-IV Axis I Disorders and provided health and psychosocial data including the Childhood Trauma Questionnaire. Repeated measures logistic regression analyses were conducted separately for women with and without lifetime MDD at study entry. Results: Among women with lifetime MDD, CM, but not current stress, interacted with menopausal status to increase the risk for MD during postmenopause (ORs ranged from 2.71 to 8.04). All stressors were associated with increased odds of MD. Among women without lifetime MDD, current stress was related to risk for MD, but the effect did not vary by menopausal status. Conclusions: Women with MDD prior to midlife and who experienced CM were at greatest risk for MD after the MT. Women without prior MDD were at increased risk for MD during peri- and postmenopause. Healthcare providers should monitor women at risk for MD even after the MT. [ABSTRACT FROM AUTHOR]