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Background: Evidence is limited regarding the role of air pollution in acute lower respiratory infections among adults. We assessed the influence of long-term air pollution exposure on hospital admission for lower respiratory infections and whether there are vulnerable subgroups., Methods: We used a populational cohort in Catalonia, Spain, comprising 3,817,820 adults residing in Catalonia as of January 1, 2015. Air pollution exposure was assigned to individuaĺs residential address using locally-developed models. We characterized the concentration-response functions between long-term air pollution exposure and hospital admission for lower respiratory infections between 2015 and 2019. We assessed interaction between exposure and clinical and socio-economic factors on multiplicative and additive scales., Results: An interquartile range exposure increase was associated with an 8 % (95 % Confidence Interval: 5 %-11 %) for Nitrogen Dioxide, 10 % (95 % Confidence Interval: 8 %-13 %) for Particulate Matter with diameter equal to or smaller than 2.5 µm, 5 % (95 % Confidence Interval: 3 %-7%) for Particulate Matter with diameter equal to or smaller than 10 µm and 18 % (95 % Confidence Interval: 14 %-22%) for ozone (adjusted by Nitrogen Dioxide) increase in hospital admissions for respiratory infections. Concentration-response functions were non-linear, with steeper slopes at exposures below the median or at most extreme high values. Associations were consistently greater for individuals over 65 years or with hypertension diagnosis and males., Conclusions: Long-term exposure to air pollution was positively associated with hospital admission for lower respiratory infections. Individuals who were older than 65 years, hypertensive or male were most vulnerable., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Cathryn Tonne reports financial support was provided by Health Effects Institute. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2025 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Objective: Factors that shape individuals' vulnerability to the effects of air pollution on COVID-19 severity remain poorly understood. We evaluated whether the association between long-term exposure to ambient NO 2 , PM 2.5 , and PM 10 and COVID-19 hospitalisation differs by age, sex, individual income, area-level socioeconomic status, arterial hypertension, diabetes mellitus, and chronic obstructive pulmonary disease., Methods: We analysed a population-based cohort of 4,639,184 adults in Catalonia, Spain, during 2020. We fitted Cox proportional hazard models adjusted for several potential confounding factors and evaluated the interaction effect between vulnerability indicators and the 2019 annual average of NO 2 , PM 2.5 , and PM 10 . We evaluated interaction on both additive and multiplicative scales., Results: Overall, the association was additive between air pollution and the vulnerable groups. Air pollution and vulnerability indicators had a synergistic (greater than additive) effect for males and individuals with low income or living in the most deprived neighbourhoods. The Relative Excess Risk due to Interaction (RERI) was 0.21, 95 % CI, 0.15 to 0.27 for NO 2 and 0.16, 95 % CI, 0.11 to 0.22 for PM 2.5 for males; 0.13, 95 % CI, 0.09 to 0.18 for NO 2 and 0.10, 95 % CI, 0.05 to 0.14 for PM 2.5 for lower individual income and 0.17, 95 % CI, 0.12 to 0.22 for NO 2 and 0.09, 95 % CI, 0.05 to 0.14 for PM 2.5 for lower area-level socioeconomic status. Results for PM 10 were similar to PM 2.5 . Results on multiplicative scale were inconsistent., Conclusions: Long-term exposure to air pollution had a larger synergistic effect on COVID-19 hospitalisation for males and those with lower individual- and area-level socioeconomic status., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: In utero exposure to bisphenols, widely used in consumer products, may alter lung development and increase the risk of respiratory morbidity in the offspring. However, evidence is scarce and mostly focused on bisphenol A (BPA) only., Objective: To examine the associations of in utero exposure to BPA, bisphenol F (BPF), and bisphenol S (BPS) with asthma, wheeze, and lung function in school-age children, and whether these associations differ by sex., Methods: We included 3,007 mother-child pairs from eight European birth cohorts. Bisphenol concentrations were determined in maternal urine samples collected during pregnancy (1999-2010). Between 7 and 11 years of age, current asthma and wheeze were assessed from questionnaires and lung function by spirometry. Wheezing patterns were constructed from questionnaires from early to mid-childhood. We performed adjusted random-effects meta-analysis on individual participant data., Results: Exposure to BPA was prevalent with 90% of maternal samples containing concentrations above detection limits. BPF and BPS were found in 27% and 49% of samples. In utero exposure to BPA was associated with higher odds of current asthma (OR = 1.13, 95% CI = 1.01, 1.27) and wheeze (OR = 1.14, 95% CI = 1.01, 1.30) (p-interaction sex = 0.01) among girls, but not with wheezing patterns nor lung function neither in overall nor among boys. We observed inconsistent associations of BPF and BPS with the respiratory outcomes assessed in overall and sex-stratified analyses., Conclusion: This study suggests that in utero BPA exposure may be associated with higher odds of asthma and wheeze among school-age girls., (Copyright © 2022. Published by Elsevier Ltd.)

Background: Urban environments are characterised by many factors that may influence children's lifestyle and increase the risk of childhood obesity, but multiple urban exposures have scarcely been studied., Objective: We evaluated the association between multiple urban exposures and childhood obesity outcomes and weight-related behaviours., Methods: We conducted a cross-sectional study including 2213 children aged 9-12 years in Sabadell, Spain. We estimated ambient air pollution, green spaces, built and food environment, road traffic and road traffic noise at residential addresses through a total of 28 exposure variables in various buffers. Childhood obesity outcomes included body mass index (BMI), waist circumference and body fat. Weight-related behaviours included diet (fast food and sugar-sweetened beverage consumption), physical activity, sedentary behaviour, sleep duration and well-being. Associations between exposures (urban environment) and outcomes (obesity and behaviours) were estimated in single and multiple-exposure regression models and in a hierarchical clustering on principal components (HCPC) analysis., Results: Forty percent of children were overweight or obese. In single exposure models, very few associations were observed between the urban exposures and obesity outcomes or weight-related behaviours after correction for multiple testing. In multiple exposure models, PM coarse , denser unhealthy food environment and land use mix were statistically significant associated with childhood obesity outcomes (e.g 17.7 facilities/km 2 increase of unhealthy food environment (OR overweight/obesity status) = 1.20 [95% CI: 1.01; 1.44]). Cluster analysis identified 5 clusters of urban exposures. Compared to the most neutral cluster, the cluster with high air pollution, road traffic, and road noise levels was associated with a higher BMI and higher odds of overweight and obesity (β (zBMI) = 0.17, [95% CI: 0.01, 0.17]; OR (overweight/obesity) = 1.36, [95% CI: 0.99, 1.85]); the clusters were not associated with the weight-related behaviours., Conclusions: This systematic study of many exposures in the urban environment suggests that an exposure pattern characterised by higher levels of ambient air pollution, road traffic and road traffic noise is associated with increased childhood obesity risk and that PM coarse , land use mix and food environment are separately associated with obesity risk. These findings require follow-up in longitudinal studies and different settings., (Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Introduction: Prenatal exposure to organochlorine compounds (OCs) can increase the risk of reported respiratory symptoms in children. It remains unclear whether these compounds can also impact on lung function. We assessed the association between prenatal exposure to OCs and lung function during childhood., Methods: We included 1308 mother-child pairs enrolled in a prospective cohort study. Prenatal concentrations of p,p'-dichlorodiphenyltrichloroethane [p,p'-DDT], p,p'-dichlorodiphenyldichloroethylene [p,p'-DDE], hexachlorobenzene [HCB], and seven polychlorinated biphenyls [PCBs] were measured in cord blood. Spirometry was performed in the offspring at ages 4 (n = 636) and 7 years (n = 1192)., Results: More than 80% of samples presented quantifiable levels of p,p'-DDE, HCB, PCB-138, PCB-153, and PCB-180; p,p'-DDE was the compound with the highest median concentrations. At 4 years, prenatal p,p'-DDE exposure was associated with a decrease in forced expiratory volume in 1 s (FEV 1 ) in all quartiles of exposure (e.g., third quartile [0.23-0.34 ng/mL]: β for FEV 1 -53.61 mL, 95% CI -89.87, -17.35, vs. the lowest). Prenatal p,p'-DDE levels also decreased forced vital capacity (FVC) and FEV 1 /FVC, but associations did not reach statistical significance in most exposure quartiles. At 7 years, p,p'-DDE was associated with a decrease in FVC and FEV 1 in only the second quartile of exposure (e.g. β for FEV 1 -36.96 mL, 95% CI -66.22, -7.70, vs. the lowest). Prenatal exposure to HCB was associated with decreased FVC and FEV 1 , but in only the second quartile and at 7 years (e.g. [0.07-0.14 ng/mL]: β for FEV 1 -25.79 mL, 95% CI -55.98, 4.39, vs. the lowest). PCBs were not consistently associated with lung function., Conclusion: Prenatal exposure to p,p'-DDE may decrease lung function during childhood, especially FEV 1 and at medium levels of exposure. Further and deeper knowledge on the impact of environmental chemicals during pregnancy on lung development is needed., (Copyright © 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Maternal diet not only provides essential nutrients to the developing fetus but is also a source of prenatal exposure to environmental contaminants. We investigated the association between dietary intake of dioxins and PCBs during pregnancy and birth size. The study included 50,651 women from the Norwegian Mother and Child Cohort Study (MoBa). Dietary information was collected by FFQs and intake estimates were calculated by combining food consumption and food concentration of dioxins, dioxin-like PCBs and non-dioxin-like PCBs. We used multivariable regression models to estimate the association between dietary intake of dioxins and PCBs and fetal growth. The contribution of fish and seafood intake during pregnancy was 41% for dietary dioxins and dioxin-like PCBs and 49% for dietary non-dioxin-like PCBs. Further stratified analysis by quartiles of seafood intake during pregnancy was conducted. We found an inverse dose-response association between dietary intake of dioxins and PCBs and fetal growth after adjustment for confounders. Newborns of mothers in the upper quartile of dioxin and dioxin-like PCBs intake had 62g lower birth weight (95% CI: -73, -50), 0.26cm shorter birth length (95% CI: -0.31, -0.20) and 0.10cm shorter head circumference (95% CI: -0.14, -0.06) than newborns of mothers in the lowest quartile of intake. Similar negative associations for intake of dioxins and dioxin-like PCBs were found after excluding women with intakes above the tolerable weekly intake (TWI=14pg TEQ/kg bw/week). The negative association of dietary dioxins and PCBs with fetal growth was weaker as seafood intake was increasing. No association was found between dietary dioxin and PCB intake and the risk for small-for-gestational age neonate. In conclusion, dietary intakes of dioxins and PCBs during pregnancy were negatively associated with fetal growth, even at intakes below the TWI., (© 2013.)

Background: Maternal exposure to polycyclic aromatic hydrocarbons (PAH) during pregnancy has been associated with reduced fetal growth. However, the role of diet, the main source of PAH exposure among non-smokers, remains uncertain., Objective: To assess associations between maternal exposure to dietary intake of the genotoxic PAH benzo(a)pyrene [B(a)P] during pregnancy and birth weight, exploring potential effect modification by dietary intakes of vitamins C, E and A, hypothesized to influence PAH metabolism., Methods: This study included 50,651 women in the Norwegian Mother and Child Cohort Study (MoBa). Dietary B(a)P and nutrient intakes were estimated based on total consumption obtained from a food frequency questionnaire (FFQ) and estimated based on food composition data. Data on infant birth weight were obtained from the Medical Birth Registry of Norway (MBRN). Multivariate regression was used to assess associations between dietary B(a)P and birth weight, evaluating potential interactions with candidate nutrients., Results: The multivariate-adjusted coefficient (95%CI) for birth weight associated with maternal energy-adjusted B(a)P intake was -20.5g (-31.1, -10.0) in women in the third compared with the first tertile of B(a)P intake. Results were similar after excluding smokers. Significant interactions were found between elevated intakes of vitamin C (>85mg/day) and dietary B(a)P during pregnancy for birth weight (P<0.05), but no interactions were found with other vitamins. The multivariate-adjusted coefficients (95%CI) for birth weight in women in the third compared with the first tertile of B(a)P intake were -44.4g (-76.5, -12.3) in the group with low vitamin C intakes vs. -17.6g (-29.0, -6.1) in the high vitamin C intake group., Conclusion: The results suggest that higher prenatal exposure to dietary B(a)P may reduce birth weight. Lowering maternal intake of B(a)P and increasing dietary vitamin C intake during pregnancy may help to reduce any adverse effects of B(a)P on birth weight., (© 2013.)

Background: Previous studies have reported maternal exposure to airborne polycyclic aromatic hydrocarbons (PAH), as well as DNA adducts reflecting total PAH exposure, to be associated with reduced fetal growth. The role of diet, the main source of PAH exposure among non-smokers, remains uncertain., Objective: To assess associations between birth weight, length and small size for gestational age (SGA) with maternal intakes of the genotoxic PAH benzo(a)pyrene [B(a)P] during pregnancy, exploring potential effect modification by dietary intakes of vitamin C, vitamin E, alpha- and beta-carotene, as well as glutathione S-transferase P1 (GSTP1) polymorphisms, hypothesized to influence PAH metabolism., Methods: 657 women in the INMA (Environment and Childhood) Project from Sabadell (Barcelona) were recruited during the first trimester of pregnancy. Dietary B(a)P and nutrient intakes were estimated from food consumption data. Genotyping was conducted for the Ile105Val variant of GSTP1. Multivariable models were used to assess associations between size at birth and dietary B(a)P, evaluating potential interactions with candidate nutrients and GSTP1 variants., Results: There were significant interactions between elevated intakes of vitamin C (above the mean of 189.41 mg/day) and dietary B(a)P during the first trimester of pregnancy in models for birth weight and length (P<0.05), but no interactions were found with other nutrients. B(a)P intakes were associated with significant reductions in birth weight and length (coefficient±SE for a 1-SD increase in B(a)P: -101.63±34.62 g and -0.38±0.16 cm, respectively) among women with low, but not high, vitamin C intakes. Elevated dietary B(a)P was also associated with increased risk of SGA births among women with low dietary vitamin C. Among these women, associations were strongest in those carrying the GSTP1 Val allele, associated with lower contaminant detoxification activity., Conclusion: Results suggest that dietary B(a)P exposure may impair fetal growth, particularly in genetically susceptible populations, and that increasing maternal intakes of vitamin C may help to reduce any adverse effects., (Copyright © 2012 Elsevier Ltd. All rights reserved.)