Summary Air pollution exposure during development was associated with food sensitization (NO x ) and atopic dermatitis (PM 2.5 ). The associations were trimester‐specific, with evidence of effect modification by extrinsic and intrinsic factors.

BACKGROUND:The familial aggregation of lung function is incompletely understood, as well as potential sex-specific patterns of associations within families. We aimed to investigate the associations of spirometry measures between parents and offspring and between siblings in two multicentre cohorts. METHODS:We studied n=1203 parent-offspring pairs and n=254 sibling pairs from the European Community Respiratory Health Survey (parents, mean age 35 years) and Respiratory Health in Northern Europe, Spain and Australia (offspring, mean age 31 years) cohorts. We used multilevel mixed-effect regression models to assess parent-offspring and between-siblings associations of forced expiratory volume in the first second (FEV1) and forced vital capacity (FVC) (litres), adjusted for sex, age, height, smoking and body mass index, accounting for clustering within centres and families. RESULTS:FEV1 and FVC were positively associated between parents and offspring (ß coef. (95% CI): FEV1 0.19 (0.14 to 0.25), FVC 0.19 (0.14 to 0.25)) and between first and second sibling (ß coef. (95% CI): FEV1 0.30 (0.17 to 0.43), FVC 0.20 (0.08 to 0.32)). The associations of FEV1 and FVC between mothers and sons were significantly higher (p<0.05) than the other sex combinations. Between siblings, FEV1 had greater concordance than FVC without evident sex-specific patterns. Results were consistent after exclusion of asthmatic participants. The proportion of variance explained within-family was 76% (95% CI 66% to 87%) for FEV1 and 80% (95% CI 69% to 91%) for FVC, after adjustment for anthropometric factors. The between-family variance was 23% (95% CI 12% to 34%) for FEV1 and 19% (95% CI 8% to 30%) for FVC. CONCLUSIONS:This study supports phenotypic concordance of lung function within families, with the strongest positive association observed between mothers and sons. Approximately 75-80% of the variance of FEV1 and FVC was explained within-family.

BACKGROUND:Black carbon (BC) is an air pollutant of growing concern due to its adverse impacts on health and climate. Growing evidence suggests that BC could have a number of negative impacts on morbidity and mortality, but more evidence is needed. OBJECTIVE:The objectives of this study are to quantify any associations between BC exposure and cause-specific (cardiovascular and cancer) mortality outcomes. METHODS:Using the Malmö Diet and Cancer Cohort linked with a high-resolution dispersion model, we examined the association between long-term exposure to locally emitted BC, nitrogen oxides (NOx) and fine particulate matter (PM2.5) with cardiovascular and cancer mortality. RESULTS:In fully adjusted models, BC exposure was consistently associated with cardiovascular mortality (HR 1.15 [1.06-1.26] per IQR increase), an association that was stronger and more robust than for PM2.5 or NOx. This association was present across all models, all time periods and both sets of exposure intervals. This association was stronger than with the other pollutants. Less clear association was found between any pollutant and cancer mortality. CONCLUSION:This study shows associations between BC exposure and especially cardiovascular mortality, consistent with international evidence showing similar impacts. For cancer mortality, there were tendencies of an association with BC but less clear than for cardiovascular mortality. These findings suggest a unique role of BC in air pollution-related cardiovascular mortality and support the need for action on mitigation of air pollution in general and BC in particular.

The Health Effects Institute recently completed an extensive research initiative to investigate novel approaches to improve assessment of long-term exposure to outdoor air pollution for health studies in North America and Europe. This overview synthesizes the key results, strengths, and limitations, along with other key research and future research needs. Exposures predicted from the various models, including those accounting for daily mobility patterns and outdoor-indoor infiltration rates, generally resulted in moderately to highly correlated exposure estimates (correlation > 0.7). Health effect estimates associated with the alternative exposures were similar, albeit with some notable differences in the magnitude – but not the direction — of the associations. This research initiative can inform decisions about estimating air pollution exposure in epidemiological studies, as investigators balance concerns about bias, efficiency, and resource needs. Future work is needed to replicate findings in other studies and regions. Other areas of future work include generating representative validation data for long-term exposure estimates, propagating exposure measurement error more fully into health effect estimates and improving understanding of the influence of indoor environments.

Background:Prenatal exposure to ambient air pollution has been linked to autism spectrum disorder (ASD), but evidence from low-exposure settings such as Denmark remains limited. Objective:We aimed to examine the association between prenatal exposure to particulate matter with a diameter of ≤2.5 µm (PM2.5), black carbon (BC), and nitrogen dioxide (NO2) and ASD in children, and to identify the most susceptible groups. Methods:We included 850,361 children born in Denmark between 1990 and 2004 and followed them for ASD diagnoses in the Danish Patient Register until age 15 years. We assigned prenatal PM2.5, BC, and NO2 levels (Danish Eulerian Hemispheric Model/Urban Background Model) at the mother's residential address at delivery, and examined the association with ASD using logistic regression with a random intercept for municipality, including interaction terms to assess effect modification by sex, maternal age, smoking status, and socioeconomic status (SES). Results:An interquartile range increase in prenatal exposure to PM2.5, BC, and NO2 was associated with ASD (adjusted odds ratio; 95% confidence interval = 1.04; 1.00-1.07 per 2.8 µg/m3, 1.05; 1.03-1.08 per 0.3 µg/m3, and 1.15; 1.11-1.19 per 8 µg/m3, respectively). The association between BC and ASD persisted even after adjusting for PM2.5. Additionally, the associations between prenatal air pollution exposure and ASD were stronger among children born to older mothers. Conclusion:We found that prenatal exposure to air pollution was associated with ASD even at the relatively low exposure levels observed in Denmark, underscoring the importance of air pollution reduction for ASD prevention. The association with BC was independent of that with PM2.5, and children born to older mothers appeared to be particularly vulnerable.

Background Father’s adolescent smoking and overweight contribute to shape future offsprings’ respiratory health. We examined whether biological aging in offspring was associated with parents’ smoking or overweight in puberty. Methods We estimated Horvath, GrimAge, PhenoAge and DunedinPACE epigenetic clocks from blood DNA methylation, in 892 RHINESSA cohort participants (mean age 27 years) with data on parental smoking and body shape in the RHINE/ECRHS surveys. Linear regressions assessed associations of parental smoking initiation ≤15 versus >15 years, and overweight body shapes in childhood/puberty versus age 30, with offspring epigenetic age acceleration, adjusting for offspring sex, age, and parental childhood socioeconomic status. Sensitivity analyses accounted for offspring smoking and BMI. Results Daughters of fathers who started smoking ≤15 years showed accelerated PCHorvath (β coefficient = 1.53; 95% confidence interval = 0.2-2.9) and PCGrimAge (1.21; 0.3-2.1), and suggestive trends in similar direction for DunedinPACE and PCPhenoAge. No corresponding associations were observed in sons. Father’s overweight in childhood/ puberty was associated with higher PCHorvath and PCPhenoAge acceleration in daughters, and higher acceleration across all clocks in sons. In analyses of sons and daughters together, paternal overweight in childhood/ puberty was associated with higher PCHorvath (2.25; 1.2-3.3), DunedinPACE (0.07; 0.01-0.1) and PCPhenoAge (3.11; 1.9–4.4). These findings remained consistent in sensitivity analyses. Mothers’s puberty exposures showed no consistent associations with offsprings’ age acceleration. Conclusions We find that smoking as well as overweight around puberty in future fathers associate with higher epigenetic age acceleration in their offspring, suggesting father’s puberty might be a susceptible period regarding offsprings’ biological aging.

BACKGROUND:Evidence suggests that a father's smoking in puberty may adversely impact respiratory health in offspring, possibly through epigenetic changes in germ cells. This study investigates whether snus use starting in or after puberty influences respiratory health in future offspring. METHODS:We analysed Swedish data from RHINE (Respiratory Health in Northern Europe) parents and RHINESSA (Respiratory Health in Northern Europe, Spain and Australia) offspring by using mixed-effect logistic regression to assess the links between paternal snus initiation around puberty and offspring asthma, chronic bronchitis, rhinitis, and eczema, adjusting for paternal and offspring smoking. RESULTS:We identified 1090 offspring-father pairs. The offspring's median age was 29 years (17-51) and 55% were women. The maternal line (n = 1421) was not analysed, as <1% of mothers used snus in puberty. The offspring of fathers starting snus use in puberty (n = 89) had a higher risk of current allergic asthma [odds ratio (OR) 1.42; 95% confidence interval (CI) 1.02-1.97], at least three asthma symptoms with allergy (OR 1.13; 95% CI 1.10-1.21), chronic bronchitis (OR 2.17; 95% CI 1.04-4.54), and eczema (OR 1.45; 95% CI 1.27-1.65). Fathers' snus use starting after puberty (n = 252) showed no consistent associations with offspring outcomes. The effect estimates were consistent after excluding offspring using snus in puberty. CONCLUSION:Paternal snus use starting in puberty was associated with a higher risk of asthma and other respiratory and allergic symptoms in offspring. These findings support the hypothesis that exposures in puberty may impact future generations' respiratory health, possibly through epigenetic changes. This highlights the need for research on exposures during this period and actions to prevent habits that could negatively impact future offspring's health.

According to the World Health Organization, all healthy pregnant women are recommended to engage in at least 150 min of regular moderate-intensity aerobic activity per week. This level of physical activity is associated with numerous physical and psychological health benefits and helps to reduce the risk of being overweight, gestational diabetes, and preeclampsia. Despite its importance, adherence to the recommended levels of physical activity is low among pregnant women in Ethiopia, particularly in urban areas. Therefore, there is a need for a better understanding of barriers and enablers that affect physical activity levels. Thus, this study explored the perceived awareness, barriers, and enablers that influence pregnant women’s physical activity in their everyday lives. Seven focus group discussions were conducted with 45 pregnant women who attended routine antenatal care visits at selected health centers in four Ethiopian cities. The data were transcribed and exported to NVivo version 14 software for data management and analysis. An inductive process of thematic analysis was employed, and themes were developed. Most of the pregnant women had awareness about the health benefits of physical activity. However, some lacked awareness regarding safety precautions and the types of physical activities that can be done during pregnancy. Additionally, some had misconceptions about physical activity throughout the first trimester, believing that it results in abortion. The preferred method of physical activity was walking, both as a means of transportation and recreation. Health conditions, personal factors (such as being office worker, time constraint lack of commitment), societal factors (such as fear of judgment, culture) and environmental factors(such as lack of paved sidewalks, unfavorable weather conditions) were identified as barriers whereas partner support, experience sharing from pregnant women who had been exercising previously and having access to green space were identified as facilitators. This study identified several barriers and enablers that influence physical activity during pregnancy. By addressing Identified barriers, policy makers can create more enabling conditions for women to engage in safe, regularphysical activity during pregnancy, thereby reducing NCDs and improving maternal wellbeing and pregnancy outcomes.

Black carbon (BC) is an air pollutant of emerging concern, and further evidence is needed to understand its health effects. This study investigates the association between gestational BC exposure and birth outcomes, and whether these effects are independent of particulate matter with an aerodynamic diameter of ≤ 2.5 μm (PM2.5) exposure. We used data from the population-based birth cohort, Maternal Air Pollution in Southern Sweden (MAPSS) for the years 2000–2009, including 43,676 mother-child pairs. Maternal exposure to air pollution at residential address was estimated using a high-resolution dispersion model. We used logistic and linear regressions to examine association of air pollution with birth outcomes adjusting for maternal age, Body Mass Index, smoking, education, maternal country of birth, sex of the child, parity, household income, and birth year. We found that BC exposure during pregnancy was associated with birth weight (decrease of 69 g per 1 µg/m³ (95

Childhood cancer aetiology is poorly understood and is considered to originate in utero and early postnatal life. In this study, we investigated perinatal characteristics as potential risk factors by performing a population-based case-control study, including 1340 cancer cases diagnosed < 19y and born between 1989-2021 in southern Sweden, and 13400 controls matched by sex, year, and municipality of birth. Perinatal characteristics were obtained from seven national registries. Cox regression was used to examine the associations between perinatal characteristics and the risk of overall childhood cancer, leukaemia, CNS tumours, lymphoma, and other cancer types combined (OCT). Large for gestational age was associated with a higher risk of overall cancer (HR, 95%CI: 1.32, 1.02-1.69) and leukaemia (HR, 95%CI: 1.58, 1.01-2.5), while a 5-min Apgar score <7 indicated a higher risk of OCT (HR, 95%CI: 2.16, 1.12-4.15). Mechanical ventilation during neonatal care was associated with a higher risk of overall cancer (HR, 95%CI: 1.88, 1.39-2.53) and OCT (HR, 95%CI: 2.09, 1.19-3.39). The aforementioned characteristics were associated with up to a threefold increased risk among children diagnosed before six months of age compared to those diagnosed later. Additionally, maternal obesity was associated with a higher risk of CNS tumours (HR, 95%CI: 1.51, 1.04-2.21) and lymphoma (HR, 95%CI: 2.26, 1.31-3.88), and maternal underweight with a higher risk of leukaemia (HR, 95%CI: 2.43, 1.40-4.22). Planned caesarean delivery indicated an increased risk of OCT (HR, 95%CI: 1.52, 1.04-2.22). Our findings identify several perinatal characteristics associated with childhood cancer risk, highlighting the perinatal period as an important window for future etiological research.

Air pollution has been linked to reduced birthweight, but the association with black carbon (BC) remains insufficiently explored. This study examined the association of gestational exposure to BC with birthweight outcomes. We included data on all singleton births in Denmark between 2004 and 2016 (n = 690,898). BC and fine particulate matter (PM2.5) were estimated by high-resolution air pollution models based on maternal residential addresses during pregnancy. Linear and Poisson regression models were employed to assess the associations of BC with birthweight, low birth weight (LBW), and small for gestational age (SGA), adjusting for spatiotemporal and individual-level covariates. Effect modification by gender, mothers' age and socio-economic status (SES) were examined. Gestational exposure to BC was associated with birthweight and SGA risk: interquartile range (0.34 μg/m3) increase in BC was associated with -9 g (95% CI: 10, -7) decrease in birthweight, a relative risk (RR) of 1.02 (1.01, 1.03) for SGA, and a RR of 1.01 (1.00, 1.03) for LBW. After further adjustment for PM2.5, the associations remained significant for birthweight, were borderline significant for SGA, and null for LBW. Associations of BC with birthweight were stronger in young mothers, in mothers with low SES, and in mothers with higher BMI. In this large nationwide study, we show that gestational exposure to BC is associated with birthweight, persisted after adjusting PM2.5, adding important new evidence supporting regulation of BC in addition to PM2.5.

BACKGROUND:Air pollution is an established risk factor for cardiovascular and metabolic diseases, but evidence on chronic kidney diseases (CKD) remains limited. OBJECTIVE:We aim to examine the association between long-term exposure to air pollutants and CKD incidence. METHODS:We followed 24,581 female nurses from the Danish Nurse Cohort, recruited in 1993 or 1999, for their first-ever hospital contact with a primary or secondary CKD diagnosis until 2018. We estimated annual mean levels of particulate matter with a diameter < 2.5 µm (PM2.5) and 10 µm (PM10), nitrogen dioxide (NO2), and black carbon (BC) at nurses' residential addresses using the DEHM/UBM/AirGIS modeling system. We used Cox regression models to examine the association of 14-year running means of air pollutants with CKD incidence and to explore the effect modification of this association by lifestyles. RESULTS:Over 521,211 person-years of follow-up, 429 nurses developed CKD. We found positive associations of modest magnitude between long-term exposure to air pollutants and CKD, with hazard ratios (95% confidence intervals) per interquartile range: 1.18 (0.93-1.50) per 2.86 µg/m3 for PM2.5, 1.14 (0.93-1.40) per 3.33 µg/m3 for PM10, 1.13 (0.99-1.28) per 8.09 µg/m3 for NO2, and 1.09 (1.00-1.20) per 0.34 µg/m3 for BC. The associations between long-term exposure to NO2 and CKD incidence were greater in never smokers than in ever-smokers. Associations with NO2 and BC remained unchanged in two-pollutant models, whereas those with PM10 and PM2.5 attenuated. SIGNIFICANCE:Our study adds important new findings to the growing evidence suggesting that air pollution may be associated with CKD incidence. IMPACT STATEMENT:This study provides longitudinal evidence that long-term exposure to ambient air pollution contributes to chronic kidney disease (CKD) incidence, even in a relatively healthy occupational cohort and at comparatively low pollution levels. Although effect sizes were modest, consistent positive associations, particularly for NO2 and black carbon, highlight traffic-related pollution as a potential renal risk factor. Stronger associations among never-smokers suggest that environmental exposures may independently influence kidney health. These findings reinforce the need to integrate air pollution into CKD risk assessment and prevention strategies. Strengthening air quality policies and reducing long-term residential exposure could help lower CKD burden and protect kidney health at the population level.

The number of people seeking help for mental illness is increasing across all ages, creating a major burden for individuals, families, and the society. While personalized medicine is advancing in other fields, diagnosis and treatment of mental disorders remain largely symptom-based and fail to capture individual, sex, and gender differences in risk, manifestation, and treatment response. Early signs of illness often go unnoticed due to the lack of monitoring tools, and stigma continues to hinder prevention and care. In some phases of life, an individual’s susceptibility to mental illness is heightened and may be influenced by changes in endocrine signalling. To address these challenges, the research project Building REsilience against MEntal illness during ENDocrine-sensitive life stages (RE-MEND) has implemented an interdisciplinary approach focusing on four critical endocrine-sensitive life stages: prenatal, puberty, peripartum, and older age. The project integrates longitudinal population-based cohorts with experimental and clinical studies to identify genetic, environmental, and endocrine factors shaping susceptibility and resilience to mental illness. Multi-omics data (genomics, epigenomics, transcriptomics, proteomics, metabolomics, lipidomics, and adductomics) will be combined with neurobiological, clinical, and behavioural measures, analysed using advanced biostatistics and machine learning. RE-MEND seeks to i) identify risk and resilience factors affecting mental health; ii) deliver biomarker panels for susceptibility, disease progression, and treatment response across sensitive life stages; iii) discover novel drug targets through repurposing strategies, and iv) promote mental health literacy and reduce stigma. The integration of biological research with communication science is anticipated to result in translatable findings, supporting earlier intervention and more effective care.

In this systematic literature review and meta-analysis, the association between air pollution exposure and depression was analyzed. This meta-analysis is based on 90 studies investigating the associations between both short- and long-term exposure to various air pollutants and depression, including post-partum depression. These studies were reported according to “The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA)” guidelines. The studies included in the meta-analysis comprised of several different air pollutants including nitrogen dioxide (NO2), sulphur dioxide (SO2), carbon monoxide (CO), particulate matter (PM2.5 and PM10), ozone (O3), and black carbon (BC), examined through both measured data and modelled estimates. A total of 17 meta-coefficients were calculated, with statistically significant associations in ten of these, indicating a clear link between air pollution exposure and depression. The meta-coefficient for long-term exposure to PM2.5 was based on 25 studies with a risk increase of 1.044 (95%: 1.024–1.064) associated with a 1 µg m−3 increase. The meta-coefficient for long-term exposure to NO2 was based on 22 studies with a risk increase of 1.011 (95%: 1.003–1.018) associated with a 1 µg m−3 increase. However, a high degree of heterogeneity throughout almost all meta-analyses may restrict the generalizability of our findings.Systematic Review Registrationhttps://inplasy.com/inplasy-2024-8-0025/, INPLASY INPLASY202480025.

Background Outdoor particulate air pollution is classified as causing lung cancer, but evidence on specific pollutants and exposure timing remains limited. Methods 22,294 participants in the population-based Malmö Diet and Cancer cohort, were enrolled between 1991 and 1996 and followed until 2016. Incident lung cancer cases were identified through national registers. Annual residential exposure to PM2.5, PM10, black carbon (BC), and nitrogen oxides (NOx) was estimated using high-resolution dispersion models and assigned based on residential history. Time-dependent Cox regression models with age as the time scale were used to estimate hazard ratios (HRs) and confidence intervals (CIs) for lung cancer incidence for exposure at baseline (1990–1994), the five years preceding diagnosis or censoring (lag 1–5), and the 6–10 years prior (lag 6–10). Models were progressively adjusted for smoking (status, intensity, duration), environmental tobacco smoke, employment, occupation, education, physical activity, cohabitation, and area-level socioeconomic status. Results During 325,966 person-years, 499 participants developed lung cancer. In models adjusted for age, sex, and calendar time, positive associations were observed for PM2.5, PM10, BC and NOx. Adjustment for smoking substantially attenuated the estimates leading to imprecise and not statistically significant associations. For example, the HR for PM2.5 (lag 1–5 years) was 1.03 (95% CI: 0.48–2.19) per 5 µg/m³, PM10 (lag 1–5 years) was 1.21 (95% CI: 0.51–2.89) per 10 µg/m³, and for BC (lag 1–5 years) was 1.10 (95% CI: 0.67–1.80) per 0.5 µg/m³, while associations with NOx were close to null. Discussion and conclusion We observed suggestive but imprecise associations between long-term PM exposure and lung cancer incidence. The attenuation after adjustment for smoking highlights the importance of careful confounder control. Overall, findings do not provide strong evidence of an independent association in this low-exposure setting and should be interpreted cautiously.

RATIONALE:Long-term exposure to air pollution contributes to chronic respiratory diseases, including asthma and chronic obstructive pulmonary disease (COPD). While the effect of fine particulate matter (PM2.5) and nitrogen dioxide (NO2) are supported by evidence, the contribution of black carbon (bc), a combustion-related pollutant, remains unclear. OBJECTIVES:To investigate associations of long-term exposure to bc as well as PM2.5 and NO2 with incidence of adult-onset asthma and COPD in Denmark. METHODS:We followed 3.2 million Danish residents aged 30 years or older on January 1, 2000 until December 31, 2018, for incidence of asthma and COPD (first hospital contact), and combined incidence (first prescription for obstructive airway disease [OAD] medication). Annual mean concentrations of air pollutants were estimated using European-wide hybrid land-use regression models. Cox proportional hazard models were used with adjustment of demographic, socioeconomic factors, smoking, and body mass index. RESULTS:During 50.7, 50.4, and 44.4 million person-years of follow-up, 52 648 participants developed asthma, 146 269 developed COPD, and 393 211 were prescribed OAD medication, respectively. An interquartile range increase of 2.0 and 10.3 µg/m3, and 0.5 × 10-5/m in PM2.5, NO2, and bc, respectively, were associated with higher risks of asthma incidence (hazard ratio: 1.10 [95% confidence interval: 1.08, 1.13]; 1.16 [1.13, 1.19]; 1.17 [1.14, 1.20]), COPD incidence (1.04 [1.02, 1.05]; 1.05 [1.03, 1.07]; 1.06 [1.04, 1.08]), and OAD medication (1.02, [1.01, 1.03]; 1.05 [1.03, 1.06]; 1.03 [1.02, 1.05]). The observed association with PM2.5 were attenuated or became null after adjusting for NO2 or bc, while those with NO2 or bc remained robust after adjusting for PM2.5. CONCLUSION:In a large Danish nationwide analysis, air pollution is an important predictor for adult-onset asthma and COPD. Our findings suggest that the relevance of pollutants originating from combustion sources, as reflected by the association with bc and NO2, may contribute importantly to these respiratory outcomes. Targeted actions to reduce combustion-related emissions, including those leading to bc formation, may further help decrease the burden of chronic respiratory diseases.

BACKGROUND:Residential greenness is linked to health, but its relationships with environmental exposures and lifestyle factors-often treated as confounders or mediators-are less clear. OBJECTIVE:We investigated the associations between residential greenness and air pollution, traffic noise and lifestyle factors (smoking, alcohol consumption, leisure-time physical activity) at six study sites in the Swedish CArdioPulmonary bioImage Study (SCAPIS), using waist circumference as an illustrative outcome. METHODS:Greenness assessment was based on the average 5-year pre-recruitment values of Normalized Difference Vegetation Index (NDVI) within 250 m buffers around participants' residences (n = 29,376; 50-65 years). We used linear regression to estimate associations between NDVI and fine particulate matter (PM2.5), respirable particulate matter (PM10), nitrogen dioxide (NO2) road traffic noise (Lden), and waist circumference; logistic regression to estimate associations between NDVI and smoking, alcohol consumption and sedentary lifestyle. RESULTS:NDVI (mean 0.47; range 0.08-0.79) varied across SCAPIS sites. Higher greenness was associated with lower air pollution and traffic noise and lower smoking and alcohol consumption, but not with sedentary lifestyle. Waist circumference (mean 89.4 cm in women; 99.7 cm in men) differed by site, but showed no independent association with greenness, after adjustment for urbanicity, site and socioeconomic variables. SCAPIS participants more often lived in urban, less green areas than the general population. SIGNIFICANCE:Greenness relates to environmental and lifestyle factors, partly in site-specific ways, underscoring the need to carefully consider what we adjust for in greenness epidemiology.

Boys’ pubertal overweight associates with future offspring’s asthma and low lung function. To identify how paternal overweight is associated with offspring’s DNA methylation (DNAm), we conducted an epigenome-wide association study of father’s body silhouette (FBS) at three timepoints (age 8, voice break and 30) and change in FBS between these times, with offspring DNAm, in the RHINESSA cohort (N = 339). We identified 2005 differentially methylated cytosine-phosphate-guanine (dmCpG) sites (FDR < 0.05), including dmCpGs associated with offspring asthma (119), lung function (178) and BMI (291). Voice break FBS associated with dmCpGs in loci including KCNJ10, FERMT1, NCK2 and WWP1 . Change in FBS across sexual maturation associated with DNAm at loci including NOP10, TRRAP, EFHD1, MRPL17 and NORD59A;ATP5B and showed strong correlation in reduced gene expression in loci NAP1L5, ATP5B, ZNF695, ZNF600, VTRNA2-1, SOAT2 and AGPAT2 . We identified 24 imprinted genes including: VTRNA2-1, BLCAP, WT1, NAP1L5 and PTPRN2 . Identified pathways relate to lipid and glucose metabolism and adipogenesis. Father’s overweight at puberty and during reproductive maturation was strongly associated with offspring DNA, suggesting a key role for epigenetic mechanisms in intergenerational transfer from father to offspring in humans. The results support an important vulnerability window in male puberty for future offspring health.

BACKGROUND:Studies on long-term exposure to air pollution at high levels suggest an association with increased risk of metabolic syndrome (MetS). We aimed to study this relationship at very low levels, less well-studied, yet of public health importance. METHODS:The Swedish CArdioPulmonary bioImage Study (SCAPIS) consists of randomly selected subjects aged 50-64 years from six large cities in Sweden (n = 30,154). Participants underwent medical examination and answered a health-related questionnaire at enrolment. MetS was defined using established criteria. Residential exposure to PM2.5 and NO2 was modelled annually for each subject over 10 years before enrolment. Adjusted prevalence ratios (adj PR) were calculated both by quartiles of exposure and per 1 μg/m3 increment in PM2.5 and NO2, with adjustments for age, lifestyle and socioeconomic factors. RESULTS:Full information on exposure, covariates, and MetS was obtained for 13,997 (90.26 %) females and 12,978 (88.61 %) males, respectively. The 10-years mean exposures of PM2.5 and NO2 before enrolment were 6.57 and 11.47 μg/m3, respectively. The prevalence of MetS was 28.75 % in females and 38.20 % in males, respectively. Quartile analysis of PM2.5 did not reveal significant increased adj PR for MetS, neither in females nor in males. For females the adj PR per 1 μg/m3 was 0.91 (0.89-0.94) and for males 0.95 (0.92-0.97), respectively. Similar, but somewhat weaker, associations were seen for NO2. CONCLUSION:Some inverse associations between air pollution and MetS were observed, but these results should be interpreted with caution due to limitations in the cross-sectional design. Results should not be interpreted beyond our studied exposure range.