Anxiety disorders (AD) are the most prevalent
psychiatric condition in the general population worldwide, and it is estimated that
between 6.57 and 13.54% of new fathers suffer from an AD (Leiferman et al.,
2021), a considerably higher proportion than the prevalence for anxiety in men
generally estimated by the World Health Organization (World Health Organization,
2017; range between 2.2 − 3.8%). The mental health of children is robustly
associated with the mental health of their parents (Jami et al., 2021). In particular,
children whose parents suffer from ADs, compared to children whose parents do
not, have a higher risk of struggling with their mental health (e.g., Connell &
Goodman, 2002; Micco et al., 2009; Lawrence et al., 2019). However, the specific
role played by fathers in children's mental health difficulties has been underinvestigated, and the particular risk posed by paternal anxiety for offspring mental health difficulties is not well understood.

Respiratory Tract Infections (RTIs) are the most common health problem in childhood, with children suffering on average 4-8 RTIs a year. Social determinants like parental education and household income, in addition to environmental and behavioural risk factors early in life, can influence susceptibility to RTI outcomes. Children living in disadvantaged socio-economic circumstances (SECs) are more likely to suffer from severe RTI outcomes, but the pathways leading to these inequalities are complex, inter-related and poorly understood. The overall objective of this project is to understand the burden of Upper and Lower Respiratory Tract Infections in children in Europe. Using federated analyses of data from the EU Child Cohort Network, the project aims to explore the social and geographic patterns and the pathways that relate social characteristics, early-life risk factors and childhood RTIs. Understanding these patterns and pathways is vital to inform preventative policy and help reduce the unfair child health differences through effective public health interventions.

One in 5 children in the United Kingdom speak two or more languages (Department of Education, 2020). Some studies have shown that bilingual children have greater mental health issues compared to monolingual children (Guhn, et. al., 2010). However, Halle et al. (2012) found that bilingual children had fewer mental health problems than their monolingual peers. Due to mixed results in the literature, it is unclear what the consequences for children’s and adolescents’ mental health when grown-up bilinguals. Using data from the Millennium Cohort Study (MCS), we have shown that bilingualism acts as a protective factor on mental health for children between 3 to 11 years old (Salgado-Garcia, Devine, & Krott, in preparation). Compared to monolingual children, bilingual children had lower levels of internalizing and externalizing problems when sex differences, nonverbal IQ, family background (SES), school characteristics, and language proficiency were taken into account. The current project aims to investigate the cognitive mechanisms underpinning the difference between bilingual and monolingual children’s mental health, specifically focus on executive functions and theory of mind.

Air pollution is the most important environmental risk factor for health, including for cardiovascular diseases (CVD), and there is growing evidence of its adverse effects on cardiovascular and metabolic health across the life course. Air pollution is the leading contributor to the global disease burden, contributing more than well established CVD risk factors, such as high systolic blood pressure, high glucose, high body mass index (BMI) and smoking.

The adverse cardiometabolic health effects of air pollution might be more pronounced among low-income, low-education, and ethnic minority groups, partly due to the generally increased air pollution exposures and the higher prevalence of risk factors for poorer cardiovascular health in socioeconomically disadvantaged populations. Therefore, a comprehensive understanding of the links between socioeconomic status (SES), ethnicity, air pollution, and health across different ages is crucial.

Postulated mechanisms linking air pollution to cardiometabolic health comprise oxidative stress, endothelial dysfunction, and inflammatory responses. Proteomics is a promising tool which enables precise identification and quantification of a range of proteins, including proteins related to chronic inflammation. Proteomics can help to characterise the complex biological processes between air pollution exposure and inflammation. Previous studies have shown that individuals with lower SES and ethnic minorities have higher levels of systemic inflammation; therefore, inflammatory pathways are likely an important mechanism for socioeconomic inequalities in the association between air pollution and cardiometabolic health.

This project aims to study socioeconomic inequalities in the cardiometabolic effects of air pollution across the life course and its potential mechanism via inflammation.

Importance and need Ambient air pollution (AAP) causes 4.2 million premature deaths globally each year. It is a major contributor to non-communicable diseases, second only to cigarette smoking. In early-life, exposure to AAP influences the long-term risk of chronic disease development. Many diseases associated with AAP, such as respiratory illnesses , originate in childhood. Poor and ethnic minority children are disproportionately affected by AAP . Effective and equitable policy interventions targeting children are thus crucial. As a vulnerable group unable to control their exposures, children need to be considered and protected in policy transitions to clean air and net-zero.
Advancing current understandings and practice To tackle the inequitable health burden of AAP, we need to advance our understanding of where early-life exposures occur and how different children may be exposed differently and/or respond differently to the same exposures. This advanced understanding needs to be incorporated into decision-support tools, most notably health impact assessments (HIA), which can then assess equity impacts of clean air and net-zero transitions. I propose building a holistic program centred on the integration of multidisciplinary data, methods, tools, and networks. This integration will enable me to innovatively capture childhood exposure to AAP, estimate novel associations with chronic disease development, create and implement an equity oriented HIA, and foster enduring strategic coalitions and partnerships. The innovation in the exposure assessment can uncover fundamental insights into exposure disparities and health effects of AAP. The equity oriented HIA tool can have transformative impact on practice and policymaking. And creating a nucleus of diverse and engaged stakeholders can amplify the program’s impact. My approach will pave the way for addressing other complex and inequitable environmental health challenges.
Timeliness and trends I have been researching AAP and its health effects, primarily in children, over the past decade. The challenge of AAP is enduring. Whilst overall AAP levels have declined in some countries including the UK, levels are still considered too high to protect human health remaining above World Health Organisation (WHO) guidelines. Net-zero policies, such vehicles electrification, are expected to reduce AAP. However, these reductions will not be enough; tempered by a large, projected increase in future demand for transport leading to potential increases in non-exhaust emissions .
General AAP reductions also mask environmental injustice where there has been no progress in reducing the exposure gap between socioeconomic and racial groups . In the UK, the exposure gap between the poor and rich even increased in what has been cited as a failure of UK air quality policy . This failure is evident at locations important for children’s health. UK schools with high annual particulate matter less than 2.5 micrometres in diameter (PM2.5) levels (>12 μgm-3) had a significantly higher intake of pupils on free school meals (17.8%) and ethnic minorities (78.3%) compared to schools with low PM2.5 (<6 μgm-3, 6.5% on free school and 6.8% ethnic minorities) . Children spend about 30% of their time in schools . Commuting to school is another major contributor to exposure that is understudied. For example, AAP during commuting was 52% higher than exposures at school on average . Commuting mode and routes dictate exposures and vary between socioeconomic and racial groups complicating the understanding of equity impacts of e.g., transport policies targeting travel to school.
There is also sporadic evidence that the most exposed children might respond differently to their AAP exposures. This can be due to higher individual susceptibility or complex interactions with environmental, lifestyle and social characteristics. For example, despite controlling for a comprehensive set of confounders, I consistently observed larger associations between AAP and asthma and wheeze in children from families who struggled financially and children from Pakistani origins in Bradford, UK. So far, I do not have a satisfactory explanation of such differences but an indication of slightly higher exposure variability in the Pakistani but not the financially strained children. The question as to whether certain children respond differently to their exposures remains challenging to answer via traditional epidemiological studies which predominantly rely on a naïve assessment of exposure at the residential address only. Such studies are the norm and incapable of accurately representing exposure variability.
Impact Advancing current understandings of where exposures occur, how exposures vary across different children, and how different children might react differently to AAP has significant implications for policymaking. It can pinpoint which environments policies need to target to be most effective (e.g., at schools, on the route to school) and reveal any differential impact of policies on subgroups who may need more prioritization through a stratified approach to prevention (e.g., ethnic minorities).
But advancing understandings without a holistic approach to drive impact will not be enough. New knowledge needs translation into a new generation of equity oriented HIA, a key aspect of my program. I will use the HIA to test various clean air and net-zero policies solicited from and designed with stakeholders, focusing on climate policies which represent pathways in motion that can reduce both pollutant and greenhouse gas emissions. This focus strategically aligns with current national and global agendas on, and large investments in, net-zero and can reorient policy to better reduce inequities. As equity is also political and multi-sectoral, I acknowledge that my vision of reducing inequity extends well beyond the provision of new scientific information or adept decision-support tools. Actively engaging with policymakers and clustering influential partners to champion children’s health, prioritize equity and uptake novel science and tools is essential and at the heart of my program.

Today, it is widely accepted that most traits are both genetically heritable and affected by the environment. In the social sciences, the previous nature-nurture debate has been replaced by a new paradigm analyzing the interplay between genetics and the social environment (e.g., in sociology: Breinholt and Conley 2023; in economics: Houmark, Ronda, and Rosholm 2024; in psychology: Wertz et al. 2020). Rooted in sociology, this project analyzes how social mechanisms of genetic effects play out in three realms affecting childhood educational performance: family, daycare, and school peers, and asks how knowledge on these social mechanisms of genetic effects changes theories of justice on social stratification. The project thereby advances knowledge on the complex interplay between the social environment and genetics and addresses ethical questions re-actualized by the integration of molecular genetics in the social sciences. Addressing these issues will promote well-being of children.

• The experience of pregnancy is associated with physiological and psychological change that is shown to promote sedentary behaviour and/or lower levels of physical activity (PA).
• PA in pregnancy has historically been deemed a risk factor for miscarriage, though this may result from reverse causality. Those feeling well enough to stay active early in pregnancy might already be in the early stages of miscarriage and thus experience fewer symptoms like nausea and fatigue. The perception of Pa as a risk may have led to the promotion of sedentary behaviour and reduced PA during pregnancy by clinicians and medical professionals in fear of causing harm.
• The majority of epidemiological analyses to-date, however, have reported that higher PA and reduced sedentary time are associated with improved health outcomes for pregnant people and their offspring. Furthermore, guidelines in several countries encourage safe levels of activity and exercise during pregnancy.
• Since PA in pregnancy may have benefits for the mother and/or offspring, it is important to better understand its effects in pregnancy on a range of pregnancy and perinatal outcomes.
• When conducting conventional multivariable regression analyses, sources of bias induced by confounding factors, including confounding by undiagnosed existing disease (reverse causation), present challenges when inferring causality.
• Mendelian randomisation (MR) exploits the random distribution of genetic variants from parents to offspring, independent of the influence from other traits, to reduce susceptibility to these confounding factors. However, MR may be biased by weak instruments or horizontal pleiotropy.
• Negative control designs, which use paternal exposures as the negative control, can reveal bias in associations of maternal exposures with adverse pregnancy and perinatal outcomes. The paternal exposure is unlikely to affect these outcomes but may be associated with unmeasured confounders in a similar way to the maternal exposure.
• Employing a triangulation approach using multivariable regression, Mendelian randomisation, and a paternal negative control design, this investigation seeks to explore the causal effects of PA in pregnancy on pregnancy and perinatal outcomes.

Lung-function impairment underlies chronic obstructive pulmonary disease (COPD) and predicts mortality. Recently, over a thousand variants in over 500 genes were associated with lung function. Those variants were involved in different cell functions, providing information that brings us closer to understanding the mechanisms underlying lung function and COPD.

In this study, we will investigate a more comprehensive number of variants in genes, with a focus on those that are not that frequent in the population (frequency under 1%), to help identifying variants responsible for lung function impairment.

*Please note this new proposal will re-use the dataset that has been provided for the previous project ID B3581.*

Polycystic ovary syndrome (PCOS) is a major health concern that affects up to 10% of reproductive-aged women and is the leading cause of female infertility. This complex, heterogenous condition is characterized by ovulatory dysfunction and hyperandrogenism and is often associated with metabolic dysregulation and increased risk for adverse birth outcomes. Existing evidence suggests that the androgenic and metabolic features of PCOS can be passed down from mothers to their offspring, but the relative contributions of maternal genetics and intrauterine environmental factors to these features in offspring are not known.

Our original project ID B3581 studies metabolic and growth and developmental phenotypes in children that may be associated with PCOS. We have recently identified that a higher polygenic risk score (PRS) for PCOS is associated with higher BMI, fat-mass index, and risk of obesity in childhood and earlier age at pubarche and younger age at peak height velocity. These associations persisted after controlling for the maternal PCOS polygenic risk score, indicating that genetic risk for PCOS has direct effects in offspring. In addition, genetic risk for PCOS could also have indirect effects in children through direct effects on the intrauterine environment in their mothers. For example, mothers with PCOS have an increased risk of preterm delivery, attributed to metabolic perinatal complications, such as pre-eclampsia.

I hypothesize that maternal PCOS genetic factors and associated intrauterine environmental factors play an integral role in the development of adverse birth outcomes and childhood androgenic and metabolic features of PCOS in offspring.