Prenatal urban environment and blood pressure trajectories from childhood to early adulthood

Ana Gonçalves Soares; Susana Santos; Emie Seyve; Rozenn Nedelec; Soile Puhakka; Aino-Maija Eloranta; Santtu Mikkonen; Wen Lun Yuan; Deborah A Lawlor; Jon Heron; Martine Vrijheid; Johanna Lepeule; Mark Nieuwenhuijsen; Serena Fossati; Vincent W V Jaddoe; Timo Lakka; Sylvain Sebert; Barbara Heude; Janine F Felix; Ahmed Elhakeem; Nicholas J Timpson

doi:10.1016/j.jacadv.2023.100808

Prenatal urban environment and blood pressure trajectories from childhood to early adulthood

Ana Gonçalves Soares^*
, Susana Santos
, Emie Seyve
, Rozenn Nedelec
, Soile Puhakka
, Aino-Maija Eloranta
, Santtu Mikkonen
, Wen Lun Yuan
, Deborah A Lawlor
, Jon Heron
, Martine Vrijheid
, Johanna Lepeule
, Mark Nieuwenhuijsen
, Serena Fossati
, Vincent W V Jaddoe
, Timo Lakka
, Sylvain Sebert
, Barbara Heude
, Janine F Felix
, Ahmed Elhakeem

Nicholas J Timpson

^*Corresponding author for this work

Research output: Contribution to journal › Article (Academic Journal) › peer-review

11 Citations (Scopus)

12 Downloads (Pure)

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
To assess associations of prenatal urban environmental exposures with blood pressure trajectories from childhood to early adulthood.

Methods
Repeated measures of systolic (SBP) and diastolic blood pressure (DBP) were collected in up to 7,454 participants from a UK birth cohort. Prenatal urban exposures (n=42) 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 four independent European cohorts (N 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 [IQR] increase in humidity: 0.29 mmHg/year, 95%CI 0.20; 0.39) and higher temperature with a slower increase (mean yearly change in SBP per IQR increase in temperature: -0.17 mmHg/year, 95%CI -0.28; -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.

Original language	English
Article number	100808
Number of pages	12
Journal	JACC Advances
Volume	3
Issue number	2
Early online date	8 Jan 2024
DOIs	https://doi.org/10.1016/j.jacadv.2023.100808
Publication status	Published - 1 Feb 2024

Bibliographical note

Funding Information:
The data that support the findings of this study are available from the authors upon reasonable request and approval from the respective cohorts executive committees. Restrictions apply to the availability of these data, which were used under license for the current study, and are not publicly available. Requests for access to ALSPAC data may be sent to the ALSPAC Executive Committee at https://proposals.epi.bristol.ac.uk/. Requests for access to the Generation R Study data can be addressed to the Director of the Core Facility Generation R ([email protected]) and will be evaluated by the Generation R Management Team taking into account local rules and regulations. Researchers interested in exploring EDEN data should contact directly [email protected] to complete a dedicated project form for evaluation by the EDEN steering committee. Requests to access NFBC data may be sent to the NFBC project centre ([email protected]). Requests for access to the PANIC study data can be addressed to [email protected]. This project received funding from the European Union's Horizon 2020 research and innovation programme (874739 LongITools; 733206 LifeCycle; 874583 ATHLETE; 824989 EUCAN-Connect; 101021566 ART-HEALTH). Drs Gonclaves Soares, Elhakeem, Lawlor, Heron, and Timpson work in a Unit that is funded by the UK Medical Research Council (MC_UU_00011/1&6) and the University of Bristol. Dr Lawlor is a National Institute of Health Research Senior Investigator (NF-0616-10102) and is also supported by a British Heart Foundation Chair (CH/F/20/90003). The UK Medical Research Council and Wellcome (Grant ref: 217065/Z/19/Z), and the University of Bristol provide core support for ALSPAC. A comprehensive list of grants funding is available on the ALSPAC website (http://www.bristol.ac.uk/alspac/external/documents/grant-acknowledgments.pdf). The general design of the Generation R Study is made possible by financial support from Erasmus MC, University Medical Center Rotterdam, Erasmus University Rotterdam, the Netherlands Organization for Health Research and Development and the Ministry of Health, Welfare and Sport. Dr Mikkonen acknowledges the Academy of Finland competitive funding to strengthen university research profiles (PROFI) for the University of Eastern Finland (grant no. 325022). The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication. Dr Lawlor reported grants from national and international government and charity funders, Roche Diagnostics, and Medtronic Ltd for work unrelated to this publication. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Publisher Copyright:
© 2024 The Authors

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 11 Sustainable Cities and Communities

Keywords

urban environment
blood pressure
ALSPAC
LongITools
cohorts
trajectories

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Soares, A. G., Santos, S., Seyve, E., Nedelec, R., Puhakka, S., Eloranta, A.-M., Mikkonen, S., Yuan, W. L., Lawlor, D. A., Heron, J., Vrijheid, M., Lepeule, J., Nieuwenhuijsen, M., Fossati, S., Jaddoe, V. W. V., Lakka, T., Sebert, S., Heude, B., Felix, J. F., ... Timpson, N. J. (2024). Prenatal urban environment and blood pressure trajectories from childhood to early adulthood. JACC Advances, 3(2), Article 100808. https://doi.org/10.1016/j.jacadv.2023.100808

@article{535ba1b5130949fc9af92be5e081bdb7,

title = "Prenatal urban environment and blood pressure trajectories from childhood to early adulthood",

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 To assess associations of prenatal urban environmental exposures with blood pressure trajectories from childhood to early adulthood. Methods Repeated measures of systolic (SBP) and diastolic blood pressure (DBP) were collected in up to 7,454 participants from a UK birth cohort. Prenatal urban exposures (n=42) 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 four independent European cohorts (N 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 [IQR] increase in humidity: 0.29 mmHg/year, 95\%CI 0.20; 0.39) and higher temperature with a slower increase (mean yearly change in SBP per IQR increase in temperature: -0.17 mmHg/year, 95\%CI -0.28; -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.",

keywords = "urban environment, blood pressure, ALSPAC, LongITools, cohorts, trajectories",

author = "Soares, \{Ana Gon{\c c}alves\} and Susana Santos and Emie Seyve and Rozenn Nedelec and Soile Puhakka and Aino-Maija Eloranta and Santtu Mikkonen and Yuan, \{Wen Lun\} and Lawlor, \{Deborah A\} and Jon Heron and Martine Vrijheid and Johanna Lepeule and Mark Nieuwenhuijsen and Serena Fossati and Jaddoe, \{Vincent W V\} and Timo Lakka and Sylvain Sebert and Barbara Heude and Felix, \{Janine F\} and Ahmed Elhakeem and Timpson, \{Nicholas J\}",

note = "Funding Information: The data that support the findings of this study are available from the authors upon reasonable request and approval from the respective cohorts executive committees. Restrictions apply to the availability of these data, which were used under license for the current study, and are not publicly available. Requests for access to ALSPAC data may be sent to the ALSPAC Executive Committee at https://proposals.epi.bristol.ac.uk/. Requests for access to the Generation R Study data can be addressed to the Director of the Core Facility Generation R ([email protected]) and will be evaluated by the Generation R Management Team taking into account local rules and regulations. Researchers interested in exploring EDEN data should contact directly [email protected] to complete a dedicated project form for evaluation by the EDEN steering committee. Requests to access NFBC data may be sent to the NFBC project centre ([email protected]). Requests for access to the PANIC study data can be addressed to [email protected]. This project received funding from the European Union's Horizon 2020 research and innovation programme (874739 LongITools; 733206 LifeCycle; 874583 ATHLETE; 824989 EUCAN-Connect; 101021566 ART-HEALTH). Drs Gonclaves Soares, Elhakeem, Lawlor, Heron, and Timpson work in a Unit that is funded by the UK Medical Research Council (MC\_UU\_00011/1\&6) and the University of Bristol. Dr Lawlor is a National Institute of Health Research Senior Investigator (NF-0616-10102) and is also supported by a British Heart Foundation Chair (CH/F/20/90003). The UK Medical Research Council and Wellcome (Grant ref: 217065/Z/19/Z), and the University of Bristol provide core support for ALSPAC. A comprehensive list of grants funding is available on the ALSPAC website (http://www.bristol.ac.uk/alspac/external/documents/grant-acknowledgments.pdf). The general design of the Generation R Study is made possible by financial support from Erasmus MC, University Medical Center Rotterdam, Erasmus University Rotterdam, the Netherlands Organization for Health Research and Development and the Ministry of Health, Welfare and Sport. Dr Mikkonen acknowledges the Academy of Finland competitive funding to strengthen university research profiles (PROFI) for the University of Eastern Finland (grant no. 325022). The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication. Dr Lawlor reported grants from national and international government and charity funders, Roche Diagnostics, and Medtronic Ltd for work unrelated to this publication. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Publisher Copyright: {\textcopyright} 2024 The Authors",

year = "2024",

month = feb,

day = "1",

doi = "10.1016/j.jacadv.2023.100808",

language = "English",

volume = "3",

journal = "JACC Advances",

issn = "2772-963X",

publisher = "Elsevier B.V.",

number = "2",

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Soares, AG, Santos, S, Seyve, E, Nedelec, R, Puhakka, S, Eloranta, A-M, Mikkonen, S, Yuan, WL, Lawlor, DA , Heron, J, Vrijheid, M, Lepeule, J, Nieuwenhuijsen, M, Fossati, S, Jaddoe, VWV, Lakka, T, Sebert, S, Heude, B, Felix, JF, Elhakeem, A & Timpson, NJ 2024, 'Prenatal urban environment and blood pressure trajectories from childhood to early adulthood', JACC Advances, vol. 3, no. 2, 100808. https://doi.org/10.1016/j.jacadv.2023.100808

TY - JOUR

T1 - Prenatal urban environment and blood pressure trajectories from childhood to early adulthood

AU - Soares, Ana Gonçalves

AU - Santos, Susana

AU - Seyve, Emie

AU - Nedelec, Rozenn

AU - Puhakka, Soile

AU - Eloranta, Aino-Maija

AU - Mikkonen, Santtu

AU - Yuan, Wen Lun

AU - Lawlor, Deborah A

AU - Heron, Jon

AU - Vrijheid, Martine

AU - Lepeule, Johanna

AU - Nieuwenhuijsen, Mark

AU - Fossati, Serena

AU - Jaddoe, Vincent W V

AU - Lakka, Timo

AU - Sebert, Sylvain

AU - Heude, Barbara

AU - Felix, Janine F

AU - Elhakeem, Ahmed

AU - Timpson, Nicholas J

N1 - Funding Information: The data that support the findings of this study are available from the authors upon reasonable request and approval from the respective cohorts executive committees. Restrictions apply to the availability of these data, which were used under license for the current study, and are not publicly available. Requests for access to ALSPAC data may be sent to the ALSPAC Executive Committee at https://proposals.epi.bristol.ac.uk/. Requests for access to the Generation R Study data can be addressed to the Director of the Core Facility Generation R ([email protected]) and will be evaluated by the Generation R Management Team taking into account local rules and regulations. Researchers interested in exploring EDEN data should contact directly [email protected] to complete a dedicated project form for evaluation by the EDEN steering committee. Requests to access NFBC data may be sent to the NFBC project centre ([email protected]). Requests for access to the PANIC study data can be addressed to [email protected]. This project received funding from the European Union's Horizon 2020 research and innovation programme (874739 LongITools; 733206 LifeCycle; 874583 ATHLETE; 824989 EUCAN-Connect; 101021566 ART-HEALTH). Drs Gonclaves Soares, Elhakeem, Lawlor, Heron, and Timpson work in a Unit that is funded by the UK Medical Research Council (MC_UU_00011/1&6) and the University of Bristol. Dr Lawlor is a National Institute of Health Research Senior Investigator (NF-0616-10102) and is also supported by a British Heart Foundation Chair (CH/F/20/90003). The UK Medical Research Council and Wellcome (Grant ref: 217065/Z/19/Z), and the University of Bristol provide core support for ALSPAC. A comprehensive list of grants funding is available on the ALSPAC website (http://www.bristol.ac.uk/alspac/external/documents/grant-acknowledgments.pdf). The general design of the Generation R Study is made possible by financial support from Erasmus MC, University Medical Center Rotterdam, Erasmus University Rotterdam, the Netherlands Organization for Health Research and Development and the Ministry of Health, Welfare and Sport. Dr Mikkonen acknowledges the Academy of Finland competitive funding to strengthen university research profiles (PROFI) for the University of Eastern Finland (grant no. 325022). The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication. Dr Lawlor reported grants from national and international government and charity funders, Roche Diagnostics, and Medtronic Ltd for work unrelated to this publication. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Publisher Copyright: © 2024 The Authors

PY - 2024/2/1

Y1 - 2024/2/1

N2 - 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 To assess associations of prenatal urban environmental exposures with blood pressure trajectories from childhood to early adulthood. Methods Repeated measures of systolic (SBP) and diastolic blood pressure (DBP) were collected in up to 7,454 participants from a UK birth cohort. Prenatal urban exposures (n=42) 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 four independent European cohorts (N 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 [IQR] increase in humidity: 0.29 mmHg/year, 95%CI 0.20; 0.39) and higher temperature with a slower increase (mean yearly change in SBP per IQR increase in temperature: -0.17 mmHg/year, 95%CI -0.28; -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.

AB - 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 To assess associations of prenatal urban environmental exposures with blood pressure trajectories from childhood to early adulthood. Methods Repeated measures of systolic (SBP) and diastolic blood pressure (DBP) were collected in up to 7,454 participants from a UK birth cohort. Prenatal urban exposures (n=42) 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 four independent European cohorts (N 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 [IQR] increase in humidity: 0.29 mmHg/year, 95%CI 0.20; 0.39) and higher temperature with a slower increase (mean yearly change in SBP per IQR increase in temperature: -0.17 mmHg/year, 95%CI -0.28; -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.

KW - urban environment

KW - blood pressure

KW - ALSPAC

KW - LongITools

KW - cohorts

KW - trajectories

U2 - 10.1016/j.jacadv.2023.100808

DO - 10.1016/j.jacadv.2023.100808

M3 - Article (Academic Journal)

C2 - 38939392

SN - 2772-963X

VL - 3

JO - JACC Advances

JF - JACC Advances

IS - 2

M1 - 100808

ER -

Prenatal urban environment and blood pressure trajectories from childhood to early adulthood

Abstract

Bibliographical note

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Keywords

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