خلاصه
تصویر مرکزی
اختصارات و کلمات اختصاری
مواد و روش ها
نتایج
بحث
نتیجه گیری
پشتیبانی مالی و افشای نویسنده
قدردانی
داده های تکمیلی
منابع
Abstract
Central Illustration
Abbreviations and Acronyms
Methods
Results
Discussion
Conclusions
Funding support and author disclosures
Acknowledgments
Supplementary data
References
چکیده
سابقه و هدف قرار گرفتن در معرض محیط شهری قبل از تولد با فشار خون در کودکان مرتبط است. پویایی این ارتباطات در دوران کودکی و سنین بعدی ناشناخته است.
اهداف: هدف از این مطالعه ارزیابی ارتباط قرار گرفتن در معرض محیط شهری قبل از تولد با مسیرهای فشار خون از کودکی تا اوایل بزرگسالی بود.
روشها اندازهگیریهای مکرر فشار خون سیستولیک (SBP) و فشار خون دیاستولیک (DBP) در 7454 شرکتکننده از یک گروه تولد در بریتانیا جمعآوری شد. قرار گرفتن در معرض شهری قبل از تولد (تعداد ¼ 43) معیارهای صدا، آلودگی هوا، محیط ساخته شده، فضاهای طبیعی، ترافیک، هواشناسی و محیط غذایی را پوشش می دهد. یک رویکرد مطالعه ارتباط گسترده در معرض استفاده قرار گرفت. مدلهای خطی با اثرات مختلط برای مدلسازی ارتباط هر مواجهه با مسیرهای فشار خون مورد استفاده قرار گرفتند. تکرار در 4 گروه مستقل اروپایی (تا 9261) جستجو شد.
نتایج: در تجزیه و تحلیلهای کشف، رطوبت بالاتر با افزایش سریعتر (میانگین تغییر سالانه SBP برای افزایش دامنه بین چارکی در رطوبت: 0.29 میلیمتر جیوه در سال، 95٪ CI: 0.20-0.39) و دمای بالاتر با افزایش آهستهتر همراه بود (میانگین تغییر سالانه SBP در هر محدوده بین چارکی افزایش دما: 0.17 میلی متر جیوه در سال، 95% فاصله اطمینان (CI): 0.28 تا 0.07) در SBP در دوران کودکی. سطوح بالاتر رطوبت و آلودگی هوا با افزایش سریع تر DBP در دوران کودکی و افزایش آهسته تر در نوجوانی همراه بود. شواهد کمی از ارتباط سایر مواجهه ها با تغییر در SBP یا DBP وجود داشت. نتایج برای رطوبت و دما، اما نه برای آلودگی هوا، در گروههای دیگر تکرار شد.
نتیجه گیری: یافته های تکراری نشان می دهد که رطوبت و دمای بالاتر قبل از تولد می تواند تغییرات فشار خون را در دوران کودکی تعدیل کند. (JACC Adv 2024; 3:100808) © 2024 The Authors. توسط الزویر به نمایندگی از بنیاد کالج قلب و عروق آمریکا منتشر شده است
Abstract
Background
Prenatal urban environmental exposures have been associated with blood pressure in children. The dynamic of these associations across childhood and later ages is unknown.
Objectives
The purpose of this study was to assess associations of prenatal urban environmental exposures with blood pressure trajectories from childhood to early adulthood.
Methods
Repeated measures of systolic blood pressure (SBP) and diastolic blood pressure (DBP) were collected in up to 7,454 participants from a UK birth cohort. Prenatal urban exposures (n = 43) covered measures of noise, air pollution, built environment, natural spaces, traffic, meteorology, and food environment. An exposome-wide association study approach was used. Linear spline mixed-effects models were used to model associations of each exposure with trajectories of blood pressure. Replication was sought in 4 independent European cohorts (up to 9,261).
Results
In discovery analyses, higher humidity was associated with a faster increase (mean yearly change in SBP for an interquartile range increase in humidity: 0.29 mm Hg/y, 95% CI: 0.20-0.39) and higher temperature with a slower increase (mean yearly change in SBP per interquartile range increase in temperature: −0.17 mm Hg/y, 95% CI: −0.28 to −0.07) in SBP in childhood. Higher levels of humidity and air pollution were associated with faster increase in DBP in childhood and slower increase in adolescence. There was little evidence of an association of other exposures with change in SBP or DBP. Results for humidity and temperature, but not for air pollution, were replicated in other cohorts.
Conclusions
Replicated findings suggest that higher prenatal humidity and temperature could modulate blood pressure changes across childhood.
Discussion
We assessed the association of 39 prenatal urban environmental exposures with blood pressure trajectories from childhood to early adulthood in ALSPAC (Central Illustration) and sought replication of the findings in 4 independent European cohorts. After accounting for multiple testing, we found that humidity was associated with faster increase in SBP and DBP in childhood, slower decrease in SBP in adulthood, and slower increase in DBP in adolescence. Temperature was associated with slower increase in SBP and DBP in childhood and faster increase in DBP in adolescence. PM2.5 was associated with faster increase in DBP in childhood and slower increase in adolescence. Little evidence for sex differences in these associations was observed. Analyses in independent cohorts replicated results for associations of humidity and temperature with change in blood pressure in childhood but not for PM2.5.
Many studies have assessed the association of outdoor temperature with blood pressure,7 but less evidence is available for humidity. In adults, humidity has been positively associated with blood pressure levels,35 and a positive association with DBP has also been observed in children.15 We were able to identify only one study which assessed the association of humidity during pregnancy with offspring blood pressure. This study, which included 1,277 European children did not find an association between prenatal humidity and blood pressure in children aged 6 to 11 years (mean difference per IQR increase in humidity: 0.76 mm Hg, 95% CI: 3.3 to 1.77 mm Hg for SBP, and 0.44 mm Hg, 95% CI: 2.79 to 1.92 mm Hg for DBP).13
Conclusions
Using an ExWAS approach to systematically assess a range of prenatal urban environmental exposures, this study showed that prenatal outdoor temperature and humidity potentially modulate blood pressure trajectories, particularly in childhood. Our study contributes to the growing body of evidence on the longitudinal associations of prenatal environmental exposures with blood pressure later in life.
ACKNOWLEDGMENTS The authors are extremely grateful to all the families who took part in this study, the midwives for their help in recruiting them, and the whole ALSPAC team, which includes interviewers, computer and laboratory technicians, clerical workers, research scientists, volunteers, managers, receptionists, and nurses. The Generation R Study is conducted by the Erasmus MC, University Medical Center Rotterdam in close collaboration with the School of Law and Faculty of Social Sciences of the Erasmus University Rotterdam, the Municipal Health Service Rotterdam area, Rotterdam, the Rotterdam Homecare Foundation, Rotterdam and the Stichting Trombosedienst & Artsenlaboratorium Rijnmond (STAR-MDC), Rotterdam. We gratefully acknowledge the contribution of children and Gonçalves Soares et al JACC: ADVANCES, VOL. 3, NO. 2, 2024 Prenatal Urban Environment and Blood Pressure Trajectories FEBRUARY 2024:100808 10 parents, general practitioners, hospitals, midwives, and pharmacies in Rotterdam. The authors thank the EDEN mother-child cohort study group, whose members are I. Annesi-Maesano, J.Y. Bernard, J. Botton, M.A. Charles, P. Dargent-Molina, B. de Lauzon-Guillain, P. Ducimetière, M. de Agostini, B. Foliguet, A. Forhan, X. Fritel, A. Germa, V. Goua, R. Hankard, B. Heude, M. Kaminski, B. Larroquey, N. Lelong, J. Lepeule, G. Magnin, L. Marchand, C. Nabet, F Pierre, R. Slama, M.J. Saurel-Cubizolles, M. Schweitzer, and O. Thiebaugeorges. They are grateful to all children and their parents and caregivers who have participated in the PANIC Study. They are also indebted to all members of the PANIC research team for their invaluable contribution in the acquisition of the data throughout the study. They also thank all NFBC1986 members and researchers who participated in the study. They also wish to acknowledge the work of the NFBC project centre.