Despite the availability of vaccinations and screenings, cervical cancer (CC) remains a major global health challenge. Understanding the factors influencing adherence to CC prevention strategies is essential, particularly among overlooked groups such as middle-aged and/or underprivileged women. For this purpose, a cross sectional study was conducted in a population comprising 379 women (aged 37 to 64 years, recruitment: 2019 to 2023) from Valencia (Spain), representing diverse socioeconomic profiles, including female sex workers (FSWs; n = 46). Data were analysed using multivariate logistic regression models. Overall, 88.65% of participants adhered to CCS recommendations and 22.16% reported past-year condom use, compared with 86.96% and 76.09%, respectively, among FSWs. In the overall population, CCS adherence was significantly associated with higher education and marginally associated with a history of candidiasis, non-condom contraceptive use in the past year, and having more children and sexual partners. Higher condom use was associated with lower alcohol consumption, being single, non-Spanish origin, not being postmenopausal, use of vaginal health products, and not previous recurrent urinary tract infections. Marginally significant positive associations were also observed for the absence of chronic disease and a history of sexually transmitted infections. Among FSWs, earlier menarche age and lower gravidity were marginally associated with higher CCS adherence, while older age at entry into prostitution and earlier sexual debut were associated with condom use, the latter marginally significant. Overall, our findings highlight the importance of further research into underprivileged groups such as midlife women across socioeconomic strata. ### Competing Interest Statement The authors have declared no competing interest. ### Funding Statement This article received funding for projects from the European Union: ATHLETE (EU874583), funded under the European Union Horizon 2020 programme, and JAPreventNCD (GA101128023), co funded by the European Union under the EU4Health Programme 2021 2027; the Ministry of Science, Innovation and Universities (Grant CNS2023145286 funded by MICIU/AEI/10.13039/501100011033 and by the European Union NextGenerationEU/PRTR); the Spanish Association Against Cancer (MICROVAGIPAP: IDEAS19098LOPE); CIBER of Epidemiology and Public Health (PAPILONGO: ESP21PI03); the General Council of Official Nursing Associations of Spain (PAPISEX: inv\_cge\_2022\_04 and inv\_cge\_2024\_14); the Foundation for the Promotion of Health and Biomedical Research of the Valencian Community (PAPILONG: UGP20242); and the Regional Ministry of Innovation, Universities, Science and Digital Society, Generalitat Valenciana (MENTABIOTA: AICO/2021/182 and CIAICO/2023/184). This work also received funding for research positions from the Carlos III Health Institute (Miguel Servet FEDER: CP20/0006 and Sara Borrell: CD23/00090, both co funded by the European Union); the Spanish Ministry of Universities (Margarita Salas Grant: MS21133); and the Regional Ministry of Innovation, Universities, Science and Digital Society (Investigo contracts: INVEST/2022/310 and INVEST/2023/219; and CIACIF/2022/268). The latter is a grant from the Programme for the Promotion of Scientific Research, Technological Development and Innovation in the Valencian Community, supporting the recruitment of predoctoral research staff and eligible for co financing by the European Social Fund. ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: Ethics Committee for Research of the General Directorate of Public Health and the Higher Centre for Research in Public Health, Valencia, Spain gave ethical approval for this work (reference numbers: 20190301/09, 20190301/09/2, 20210604/10/02) I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable. Yes The data supporting the findings of this study are available upon request.

OBJECTIVE:To assess secular trend in age at menarche spanning nearly eight decades and to explore variations in these patterns according to selected sociodemographic and anthropometric determinants in the Valencian Community, Spain. MATERIALS AND METHODS:This population-based study included 417 260 participants born between 1931 and 2008. First, secular trend in age at menarche were assessed using time-series models across 5-year birth cohorts for the overall population. Then, 5-year birth cohorts were combined into two groups based on the data availability for the determinant analyses: an earlier-born group (1941-1975), whose age at menarche was reported retrospectively in adulthood, and a later-born group (1991-2005), whose age at menarche was collected during childhood and/or adolescence. Bayesian linear regression models were fitted for each group, adjusting for 5-year birth cohort and continent of birth in all models, and additionally for educational level in the earlier-born group and body mass index (BMI) in the later-born group. RESULTS:Mean age at menarche decreased by 1.9 years, from 13.1 to 11.1, between the 1931-1935 and 2006-2008 birth cohorts, with a steeper decline after 1975. Compared with European-born participants, those born in South/Central America (β [95% CI]: 0.33 [0.30, 0.36] years) and Africa (0.52 [0.45, 0.58] years) experienced later menarche in the earlier-born group, whereas those born in South/Central America experienced earlier menarche in the later-born group (-0.18 [-0.28, -0.09] years). In the later-born group, lower BMI was associated with later menarche (0.96 [0.74, 1.18] years) whereas higher BMI with earlier onset (-0.53 [-0.57, -0.48] years). CONCLUSION:There was a marked decline in age at menarche in the Valencian Community. Factors associated with age at menarche included continent of birth (with cohort-specific effects) and BMI.

Background: Menarche is a critical developmental milestone, with earlier onset associated with adverse long-term health consequences. Despite a reported global decline in age at menarche over the last century, this trend and its determinants remain insufficiently studied in Spain. Objective: To assess secular trends in age at menarche and its determinants in the Valencian Community, Spain. Methods: This population-based study included 417,260 participants born between 1931 and 2008. First, secular trends in age at menarche were assessed using time-series models across 5-year birth cohorts for the overall population. Then, participants were categorized as either women (born 1931-1985) or girls (born 1990-2008), and Bayesian linear regression models were fitted for each group, adjusting for birth cohort and continent of birth in all models, and additionally for educational level in women and body mass index (BMI) in girls. Results: Mean age at menarche decreased by 1.9 years, from 13.1 to 11.1, between the 1931-1935 and 2006-2008 birth cohorts, with a steeper decline after 1975. Compared to Europeans, women born in South/Central America (β[95% CI]: 0.33[0.30, 0.36] years) and Africa (0.52[0.45, 0.58] years) experienced later menarche, while girls from South/Central America experienced earlier onset (-0.18[-0.28, -0.09] years). In girls, lower BMI was associated with later menarche (0.96[0.74, 1.18] years) and higher BMI with earlier onset (-0.53[-0.57, -0.48] years). Conclusion: There was a marked decline in age at menarche in the Valencian Community, with no evidence of leveling off. Key determinants included continent of birth (with cohort-specific effects) and BMI. ### Competing Interest Statement The authors have declared no competing interest. ### Funding Statement This article received funding from multiple sources. European Union funding was provided through the ATHLETE project (Grant Agreement No. 874583) under the Horizon 2020 programme, and the JAPreventNCD project (Grant Agreement No. 101128023), co-funded by the EU4Health Programme 2021-2027. Additional funding was provided by Spanish institutions, including the Ministry of Science, Innovation and Universities (Grant CNS2023-145286, funded by MICIU/AEI/10.13039/501100011033 and by the European Union NextGenerationEU/PRTR); the Spanish Association Against Cancer (MICROVAGIPAP: IDEAS19098LOPE); the CIBER of Epidemiology and Public Health (PAPILONGO: ESP21PI03); the General Council of Official Nursing Associations of Spain (PAPISEX: inv\_cge\_2022_04); the Foundation for the Promotion of Health and Biomedical Research of the Valencian Region (PAPILONG: UGP-20-242); the Regional Ministry of Innovation, Universities, Science and Digital Society of the Generalitat Valenciana (MENTABIOTA: AICO/2021/182 and CIAICO/2023/184); and the Fundacio La Marato (202414). In addition, this article was supported by funding for research positions from the Carlos III Health Institute (Miguel Servet-FEDER: CP11/00178, MSII16/00051, CP20/0006, and Sara Borrell: CD23/00090, all co-funded by the European Union), as well as the Regional Ministry of Innovation, Universities, Science and Digital Society (Investigo contracts: INVEST/2022/310 and CIACIF/2022/268). The latter corresponds to a grant from the Programme for the Promotion of Scientific Research, Technological Development and Innovation in the Valencian Community, supporting the recruitment of predoctoral research staff and eligibility for co-financing by the European Social Fund. ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: All study protocols, including two secondary population-based registries and two datasets collected by the research team, were approved by the Directorate of Public Health and the Higher Centre for Research in Public Health (DGSP-CSISP) Ethics Committee from Valencia (references numbers: 20180112/03; 20190329/3; 20190301/09/1; and 20210604/10/01). Secondary data were provided anonymized, while investigator-collected data were anonymized prior to analysis following written informed consent from participants or legal guardians (for minors). All procedures were conducted in accordance with the Declaration of Helsinki. I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable. Yes Data from population-based registries (Valencian Breast Cancer Screening Program and the Ambulatory Care Information System of the Valencian Health Agency) are not publicly available due to ethical and legal restrictions related to the use of sensitive health data, and access is restricted. Data from the INMA and PAPILONG cohort studies are available upon request to the corresponding author and in accordance with the applicable data access procedures and ethical approvals. The INMA cohort data are subject to the INMA collaboration policy (https://www.proyectoinma.org/en/inma-project/inma-collaborationpolicy/).

Puberty relies on a hormone-regulated cascade of events initiated in fetal life and might be disrupted by prenatal exposure to endocrine-disrupting chemicals (EDCs), with alterations manifesting during pubertal development. However, studies addressing prenatal exposure to multiple EDCs remain scarce. This study explores the associations between prenatal exposure to 33 EDCs and early sex maturation in 386 Spanish mother-child pairs (girls: 49%; recruitment: 2003-2005). We measured seven organochlorine compounds (OCs) and four perfluoroalkyl substances (PFAS) in maternal blood, and seven phenols and 15 phthalates in maternal urine. Pubertal development was assessed at age 9 using Tanner staging for genital development (GD), breast development (BD), and pubic hair development (PH) alongside salivary sex hormones. Sex-specific analyses included single-chemical (robust Poisson/linear regression) and mixture (principal components/Bayesian kernel machine regression) analyses. In single-chemical models, higher prenatal p,p'-DDE and p,p'-DDT concentrations were associated with delayed BD and GD, respectively, while PCB-180 and parabens (ETPA, BUPA) were associated with earlier BD, and phthalates were associated with earlier PH (girls: MEHP, MEHHP, MEOHP, and MECPP; boys: MEP and MnBP). For sex hormones, β-HCH (both sexes), p,p'-DDE, PCB-180, PFOS (boys), and p,p'-DDT, OH-MPHP (girls) were positively associated with testosterone, and HCB was positively associated with estradiol (boys). Conversely, BUPA, OH-MPHP (boys), and BPA (girls) were inversely associated with testosterone. In chemical mixture models, the first component of OCs was positively associated with male testosterone, but the results of other mixture analyses were unclear. Overall, prenatal exposure to some EDCs may impair fetal programming of puberty, yet the impact of chemical mixtures remains uncertain.

Survivorship (or selection) bias arises within statistical analyses where the observed data are subject to some underlying selection process prior to entry into the sampled data. For example, within capture-recapture studies, a primary selection mechanism is the survival until initial capture time. The common Cormack-Jolly-Seber model conditions on the first time an individual is observed, leading to potential survivorship bias. However, while the issue of survivorship bias has been well studied in many fields, there has been little exploration within the capture-recapture framework. In particular, we focus on individual (continuous) random effect Cormack-Jolly-Seber models, where it is assumed that individuals have different survival probabilities, specified to be from some common underlying distribution. We discuss the implications of the survivorship bias within the data collection process, and describe a novel modeling approach that accounts for the survivorship bias within an ecologically sensible manner. Using simulated data, we demonstrate the significant impact of ignoring the survivorship bias present in the data. We fit the corrected model to a guillemot data set and demonstrate that even with relatively mild selection bias, the individual heterogeneity variability is substantially underestimated when ignoring this survivorship bias.

BackgroundWe aimed to explore associations between the presence of pets at one and 4-5 years of age with internalizing and externalizing problems at 7-8 years.MethodsParticipants comprised 1893 families from the INfancia y Medio Ambiente (INMA) project. Information was collected on the presence of (1) any pet, (2) dogs, (3) cats, (4) birds or (5) other animals. Pet ownership was categorized as never, always, only at age 1 and only at age 4-5. Internalizing and externalizing problems were measured at ages 7-8 years through the Strengths and Difficulties Questionnaire, a Likert questionnaire on children's behavioural and emotional symptoms. Negative binomial regression models and Tukey's multiple comparison tests were used to analyse data sets. Five sensitivity analyses were performed.ResultsFamilies that always owned a pet made up 24.4% of the sample. In addition, 11.5%, 4.5%, 3.8% and 17.6% of the families owned a dog, cat, bird or other animal, respectively. The median (P25-P75) for internalizing problems was 3 (1-5) and 5 (3-8) for externalizing problems. Owning a cat only at age 4-5 increased mental health problems: relative rate ratio (RRR) [95% confidence interval (CI)] 1.37 (1.05-1.79) for internalizing and 1.26 (1.02-1.56) for externalizing. Always having other animals was a protective factor for internalizing problems with an RRR of 0.80 (0.66-0.96). These associations remained after multiple comparison testing and sensitivity analyses.ConclusionOwning a cat only at 4-5 years of age was linked to more internalizing and externalizing problems, whereas always having other animals was a protective factor against internalizing problems.

The objective is to investigate the relation between cord blood mercury concentrations and child neurobehavioural functioning assessed longitudinally during childhood until pre -adolescence. Methods: The study involves mothers and their offspring engaged in the Spanish INMA birth cohort (n = 1147). Total mercury (THg) was determined in cord blood. Behavioural problems were assessed several times during childhood using the ADHD-DSM-IV at age 4, SDQ at ages 7 and 11, CPRS-R:S and the CBCL at ages 7, 9 and 11. Covariates were obtained through questionnaires during the whole period. Multivariate generalised negative binomial (MGNB) models or mixed -effects MGNB (for those tests with information at one or more time points, respectively) were used to investigate the relation between cord blood THg and the children 's punctuations. Models were adjusted for prenatal fish intake. Effect modification by sex, prenatal and postnatal fish intake, prenatal fruit and vegetable intake, and maternal polychlorinated biphenyl concentrations (PCBs) was assessed by interaction terms. Results: The geometric mean +/- standard deviation of cord blood THg was 8.22 +/- 2.19 mu g/L. Despite adjusting for fish consumption, our results did not show any statistically significant relationship between prenatal Hg and the children 's performance on behavioural tests conducted between the ages of 4 and 11. Upon assessing the impact of various factors, we observed no statistically significant interaction. Conclusion: Despite elevated prenatal THg exposure, no association was found with children's behavioural functioning assessed from early childhood to pre -adolescence. The nutrients in fish could offset the potential neurotoxic impact of Hg. Further birth cohort studies with longitudinal data are warranted.

BACKGROUND:There is limited epidemiological evidence on the association of prenatal exposure to phthalates and synthetic phenols with altered pubertal timing. OBJECTIVE:To examine the association of prenatal exposure to phthalates, bisphenol A (BPA), parabens, benzophenone 3 (BP-3), and triclosan (TCS) with pubertal development in girls and boys from three European cohorts. METHODS:Urinary metabolites of six different phthalate diesters (DEP, DiBP, DnBP, BBzP, DEHP, and DiNP), BPA, methyl- (MePB), ethyl- (EtPB), propyl- (PrPB), and butyl-paraben (BuPB), BP-3, and TCS were quantified in one or two (1st and 3rd trimester) urine samples collected during pregnancy (1999-2008) from mothers in three birth cohorts: INMA (Spain), EDEN (France), and MoBa (Norway). Pubertal development of their children was assessed at a single visit at age 7-12 years (579 girls, 644 boys) using the parent-reported Pubertal Development Scale (PDS). Mixed-effect Poisson and g-computation and Bayesian Kernel Machine Regression (BKMR) were employed to examine associations of individual and combined prenatal chemical exposure, respectively, with the probability of overall pubertal onset, adrenarche, and gonadarche (stage 2+) in girls and boys. Effect modification by child body mass index (BMI) was also assessed. RESULTS:Maternal concentrations of the molar sum of DEHP and of DiNP metabolites were associated with a slightly higher probability of having started puberty in boys (relative risk, RR [95% CI] = 1.13 [0.98-1.30] and 1.20 [1.06-1.34], respectively, for a two-fold increase in concentrations), with a stronger association for DiNP in boys with overweight or obesity. In contrast, BPA, BuPB, EtPB, and PrPB were associated with a lower probability of pubertal onset, adrenarche, and/or gonadarche in all boys (e.g. overall puberty, BPA: RR [95% CI] = 0.93 [0.85-1.01] and BuPB: 0.95 [0.90-1.00], respectively), and the association with BPA was stronger in boys with underweight/normal weight. In girls, MEHP and BPA were associated with delayed gonadarche in those with underweight/normal weight (RR [95% CI] = 0.86 [0.77-0.95] and 0.90 [0.84-0.97], respectively). Most of these associations were trimester specific. However, the chemical mixture was not associated with any pubertal outcome in boys or girls. CONCLUSIONS:Prenatal exposure to certain phthalates and synthetic phenols such as BPA may impact the pubertal development of boys, and weight status may modify this effect. BPA may also alter the pubertal development of girls.

With the branding of a city as green increasingly serving to amplify attractiveness andinvestment while also contributing to patterns of green gentrification, the incentive to link real estate development and green space is growing. Yet, little is known about the extent to which this incentive has generated a spatial relationship between green space and newly constructed housing at the city-wide level and in ways that can be compared between cities. This gap in knowledge makes it difficult to precisely indicate the implications for housing rights, affordability, and broader goals of urban green justice. In response, this study explores quantitative trends in 26 mid-sized North American and European cities, utilizing greening and real estate data from the last three decades. Results show that greening becomes a more significant driver of development over time and operates to attract development in a growing number of cities, although more so in US cities. Next, in order to contextualize the quantitative results, we employ qualitative field data gathered through field work in Atlanta and Amsterdam. We contrast the greening and development trajectories of these cities by examining implications for housing rights and social justice, accounting for the fact that those cities exhibit different green gentrification trends, as demonstrated in the literature. Green gentrification is indeed a proxy for understanding housing justice impli- cations in the relationship between greening and development. We find that Amsterdam's legacy of housing rights and policies acts as a protection against growing inequities embedded in the relationship between urban greening, development, and gentrification. In contrast, Atlanta embodies patterns of historic racial segregation and continued gentrification of Black neighborhoods which urban greening has further intensified. This analysis shows that greening can attract real estate development across a city, but the implications need not always be harmful to social equity.

We consider the challenges that arise when fitting ecological individual heterogeneity models to "large" data sets. In particular, we focus on dividual heterogeneity present in ecological populations within the context of capture-recapture data, although the approach is more widely applicable to more general latent variable models. Within such models the associated likelihood is expressible only as an analytically intractable integral. Common techniques for fitting such models to data include, for example, the use of numerical approximations for the integral or a Bayesian data augmentation approach. However, as the size of the data set increases (i.e., the number of individuals increases), these computational tools may become computationally infeasible. We present an efficient Bayesian model-fitting approach, whereby we initially sample from the posterior distribution of a smaller subsample of the data, before correcting this sample to obtain estimates of the posterior distribution of the full data set using an importance sampling approach. We consider several practical issues, including the subsampling mechanism, computational efficiencies (including the ability to parallelise the algorithm) and combining subsampling estimates using multiple subsampled data sets. We initially demonstrate the feasibility (and accuracy) of the approach via simulated data before considering a challenging real data set of approximately 30,000 guillemots and, using the proposed algorithm, obtain posterior estimates of the model parameters in substantially reduced computational time, compared to the standard Bayesian model-fitting approach.

Climate warming can reduce food resources for animal populations. In species exhibiting parental care, parental effort is a 'barometer' of changes in environmental conditions. A key issue is the extent to which variation in parental effort can buffer demographic rates against environmental change. Seabirds breed in large, dense colonies and globally are major predators of small fish that are often sensitive to ocean warming. We explored the causes and consequences of annual variation in parental effort as indicated by standardised checks of the proportions of chicks attended by both, one or neither parent, in a population of common guillemots Uria aalge over four decades during which there was marked variation in marine climate and chick diet. We predicted that, for parental effort to be an effective buffer, there would be a link between environmental conditions and parental effort, but not between parental effort and demographic rates. Environmental conditions influenced multiple aspects of the prey delivered by parents to their chicks with prey species, length and energy density all influenced by spring sea surface temperature (sSST) in the current and/or previous year. Overall, the mean annual daily energy intake of chicks declined significantly when sSST in the current year was higher. In accordance with our first prediction, we found that parental effort increased with sSST in the current and previous year. However, the increase was insufficient to maintain chick daily energy intake. In contrast to our second prediction, we found that increased parental effort had major demographic consequences such that growth rate and fledging success of chicks, and body mass and overwinter survival of breeding adults all decreased significantly. Common guillemot parents were unable to compensate effectively for temperature-mediated variation in feeding conditions through behavioural flexibility, resulting in immediate consequences for breeding population size because of lower adult survival and potentially longer-term impacts on recruitment because of lower productivity. These findings highlight that a critical issue for species' responses to future climate change will be the extent to which behavioural buffering can offer resilience to deteriorating environmental conditions.

Seabirds are bioindicators of marine ecosystems health and one of the world's most endangered avian groups. The creation of marine protected areas plays an important role in the conservation of marine environment and its biodiversity. The distributions of top predators, as seabirds, have been commonly used for the management and creation of these figures of protection. The main objective of this study is to investigate seabirds biodiversity distribution in the Mediterranean Sea through the use of Bayesian spatial Beta regression models. We used an extensive historical database of at-sea locations of 19 different seabird species as well as geophysical, climatology variables and cumulative anthropogenic threats to model species biodiversity. We found negative associations between seabirds biodiversity and distance to the coast as well as concavity of the seabed, and positive with chlorophyll and slope. Further, a positive association was found between seabirds biodiversity and coastal impact. In this study we define as hot spot of seabird biodiversity those areas with a posterior predictive mean over 0.50. We found potential hot spots in the Mediterranean Sea which do not overlap with the existing MPASs and marine IBAs. Specifically, our hot spots areas do not overlap with the 52.04% and 16.87% of the current MPAs and marine IBAs, respectively. Overall, our study highlights the need for the extension of spatial prioritization of conservation areas to seabirds biodiversity, addressing the challenges of establishing transboundary governance.

Early exposure to mercury has been related to endocrine disruption. Steroid hormones play a crucial role in neural cell migration, differentiation, etc., as well as protecting against several neurotoxic compounds. We investigate the relation between mercury exposure and children's sexual development, and we evaluate the possible influence of different brain-derived neurotrophic factor (BDNF) polymorphisms on this association. Our study sample comprised 412 9-year-old children participating in the INMA cohort (2004-2015). Mercury concentrations were measured at birth (cord blood) and at 4 and 9 years of age (hair). Sexual development was assessed by levels of sex steroid hormones (estradiol and testosterone) in saliva and the Tanner stages of sex development at 9 years (categorized as 1: prepuberty and >1: pubertal onset). Covariates and confounders were collected through questionnaires during pregnancy and childhood. Polymorphisms in the BDNF gene were genotyped in cord blood DNA. Multivariate linear regression analyses were performed between mercury levels and children's sexual development by sex. Effect modification by genetic polymorphisms and fish intake was assessed. We found marginally significant inverse associations between postnatal exposure to mercury (at 9 years) and testosterone levels (p[95%CI] = -0.16[-0.33,0.001], and -0.20[-0.42,0.03], for boys and girls, respectively). Additionally, we found that prenatal mercury was negatively associated with Tanner stage >1 in boys. Finally, we found significant genetic interactions for some single nucleotide polymorphisms in the BDNF gene. In conclusion, pre and postnatal exposure to mercury seems to affect children's sexual development and BDNF may play a role in this association, but further research would be needed.

Results of studies on perfluoroalkyl substances (PFASs) and thyroid hormones (THs) are heterogeneous, and the mechanisms underlying the action of PFASs to target THs have not been fully characterized. We examined the relation between first-trimester maternal PFAS and TH levels and the role played by polymorphisms in the iodothyronine deiodinase 1 (DIO1) and 2 (DIO2) genes in this association. Our sample comprised 919 pregnant Spanish women (recruitment = 2003-2008) with measurements of perfluorohexanesulfonic acid (PFHxS), perfluorooctanoic acid (PFOA), perfluorooctanesulfonic acid (PFOS), perfluorononanoic acid (PFNA), thyroid-stimulating hormone (TSH), total triiodothyronine (TT3), and free thyroxine (FT4), and we genotyped for single-nucleotide polymorphisms in the DIO1 (rs2235544) and DIO2 (rs12885300) genes. We performed multivariate regression analyses between PFASs and THs and included the interaction term PFAS-genotypes in the models. PFHxS was associated with an increase in TSH (% change in outcome [95% CI] per 2-fold PFAS increase = 6.09 [-0.71, 13.4]), and PFOA and PFNA were associated with a decrease in TT3 (-7.17 [-13.5, -0.39] and -6.28 [-12.3, 0.12], respectively). We found stronger associations between PFOA, PFNA, and TT3 for DIO1-CC and DIO2-CT genotypes, although interaction p-values were not significant. In conclusion, this study found evidence of an inverse association between PFOA and TT3 levels. No clear effect modification by DIO enzyme genes was observed.

We consider the challenges that arise when fitting complex ecological models to “large” data sets. In particular, we focus on random effect models which are commonly used to describe individual heterogeneity, often present in ecological populations under study. In general, these models lead to a likelihood that is expressible only as an analytically intractable integral. Common techniques for fitting such models to data include, for example, the use of numerical approximations for the integral, or a Bayesian data augmentation approach. However, as the size of the data set increases (i.e. the number of

Although urban greening is universally recognized as an essential part of sustainable and climate-responsive cities, a growing literature on green gentrification argues that new green infrastructure, and greenspace in particular, can contribute to gentrification, thus creating social and racial inequalities in access to the benefits of greenspace and further environmental and climate injustice. In response to limited quantitative evidence documenting the temporal relationship between new greenspaces and gentrification across entire cities, let alone across various international contexts, we employ a spatially weighted Bayesian model to test the green gentrification hypothesis across 28 cities in 9 countries in North America and Europe. Here we show a strong positive and relevant relationship for at least one decade between greening in the 1990s-2000s and gentrification that occurred between 2000-2016 in 17 of the 28 cities. Our results also determine whether greening plays a "lead", "integrated", or "subsidiary" role in explaining gentrification.

Background: Prenatal arsenic (As) exposure could negatively affect child neuropsychological development, but the current evidence is inconclusive. Objectives: To explore the relationship between prenatal urinary total As (TAs) concentrations, the As species and the methylation efficiency, and child neuropsychological development in a Spanish birth cohort. We also studied the effect modification produced by sex and several nutrients and elements. Materials and methods: Study subjects were 807 mother-child pairs participating in the INMA (Childhood and Environment) Project. Urinary TAs and its metabolites, monomethylarsonic acid (MMA), dimethylarsinic acid (DMA), inorganic As (iAs) and arsenobetaine were measured in the first trimester of pregnancy. Methylation efficiency was determined through the percentages of the metabolites and using principal component analysis. Children's neuropsychological development was assessed at the age of 4-5 years using the McCarthy Scales of Children's Abilities (MSCA). Multivariable linear regression models were built to assess the association between TAs, the As species and the maternal methylation efficiency, and the neuropsychological scores. We explored effect modification by sex, iron status, maternal nutrients status (serum manganese and selenium, and urinary zinc), and maternal vitamins intake (folate, and vitamins B-12 and B-6). Results: The geometric mean (95%CI) of Sigma(As) (sum of DMA, MMA and iAs) was 7.78 (7.41, 8.17) mu g/g creatinine. MMA concentrations were inversely associated with the scores for the general, verbal, quantitative, memory, executive function and working memory scales (i.e. beta [CI95%] = -1.37 [-2.33, -0.41] for the general scale). An inverse association between %MMA and the memory scores was found. Children whose mothers had lower manganese, zinc and ferritin concentrations obtained lower scores on several MSCA scales with decreasing As methylation efficiency. Discussion: An inverse association was observed between MMA concentrations and children's neuropsychological development. Maternal levels of manganese, zinc and ferritin affected the association between As methylation efficiency and MSCA scores.

Although cities globally are increasingly mobilizing re-naturing projects to address diverse urban socio-environmental and health challenges, there is mounting evidence that these interventions may also be linked to the phenomenon known as green gentrification. However, to date the empirical evidence on the relationship between greenspaces and gentrification regarding associations with different greenspace types remains scarce. This study focused on 28 mid-sized cities in North America and Western Europe. We assessed improved access to different types of greenspace (i.e. total area of parks, gardens, nature preserves, recreational areas or greenways [i] added before the 2000s or [ii] added before the 2010s) and gentrification processes (including [i] gentrification for the 2000s; [ii] gentrification for the 2010s; [iii] gentrification throughout the decades of the 2000s and 2010s) in each small geographical unit of each city. To estimate the associations, we developed a Bayesian hierarchical spatial model for each city and gentrification time period (i.e. a maximum of three models per city). More than half of our models showed that parks-together with other factors such as proximity to the city center-are positively associated with gentrification processes, particularly in the US context, except in historically Black disinvested postindustrial cities with lots of vacant land. We also find than in half of our models newly designated nature preserves are negatively associated with gentrification processes, particularly when considering gentrification throughout the 2000s and the 2010s and in the US. Meanwhile, for new gardens, recreational spaces and greenways, our research shows mixed results (some positive, some negative and some no effect associations). Considering the environmental and health benefits of urban re-naturing projects, cities should keep investing in improving park access while simultaneously implementing anti-displacement and inclusive green policies.

Previous literature on prenatal phenol exposure and thyroid hormone (TH) alteration is conflicting, and the possible mechanisms of action involved remain unclear. We aimed to examine the association between prenatal phenol exposure and levels of maternal and neonatal THs, as well as the possible role of iodothyronine deiodinase (DIO) gene polymorphisms in this relation. We studied 387 Spanish mother-neonate pairs with measurements of maternal phenols, total triiodothyronine (TT3) and free thyroxine (FT4), maternal and neonatal thyroid-stimulating hormone (TSH), and maternal genotypes for single nucleotide polymorphisms in the DIO1(rs2235544) and DIO2(rs12885300) genes. We implemented multivariate linear and weighted quantile sum (WQS) regressions to examine the association between phenols and THs (including sex-stratified models for neonatal TSH) and investigated effect modification of genotypes in the maternal phenol-TH associations. In single exposure models, we found negative associations between maternal triclosan (TCS) and neonatal TSH (% change [95%CI]: -2.95 [-5.70, -0.11], per twofold phenol increase) - stronger for girls - and less clearly for maternal ethylparaben (EPB) and TSH (-2.27 [-4.55, 0.07]). In phenol mixture models, we found no association with THs. In the genetic interaction models, we found some evidence of effect modification of DIO gene polymorphisms with stronger negative associations between methylparaben (MPB), propylparaben (PPB), butylparaben (BPB) and TT3 as well as bisphenol A (BPA) and FT4 for DIO1(rs2235544)-CC. Stronger inverse associations for genotypes DIO2(rs12885300)-CC and DIO2(rs12885300)-CT and positive ones for DIO2(rs12885300)-TT were also reported for BPA and FT4. In conclusion, we found some evidence of an association between phenols and TSH during pregnancy and at birth in single exposure models, the latter being stronger for girls. Since no association was observed between maternal levels of phenols and TT3 or FT4, the possible role of the genetic background in these associations warrants further investigation.