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BACKGROUND: Though observational studies have widely linked air pollution exposure to various chronic diseases, evidence comparing different exposures in the same people is limited. This study examined associations between changes in air pollution exposure due to relocation and the incidence and mortality of 14 major diseases. METHODS: We included 50,522 participants enrolled in the UK Biobank from 2006 to 2010. Exposures to particulate matter with a diameter [less than or equal to]2:5 lm (P[M.sub.2:5]), particulate matter with a diameter [less than or equal to]10 lm (P[M.sub.10]), nitrogen oxides (N[O.sub.x]), nitrogen dioxide (N[O.sub.2]), and sulfur dioxide (S[O.sub.2]) were estimated for each participant based on their residential address and relocation experience during the follow-up. Nine exposure groups were classified based on changes in long-term exposures due to residential mobility. Incidence and mortality of 14 major diseases were identified through linkages to hospital inpatient records and death registries. Cox proportional hazard models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for incidence and mortality of the 14 diseases of interest. RESULTS: During a median follow-up of 12.6 years, 29,869 participants were diagnosed with any disease of interest, and 3,144 died. Significantly increased risk of disease and all-cause mortality was observed among individuals who moved from a lower to higher air polluted area. Compared with constantly low exposure, moving from low to moderate P[M.sub.2:5] exposure was associated with increased risk of all 14 diseases but not for all-cause mortality, with adjusted HRs (95% CIs) ranging from 1.18 (1.05, 1.33) to 1.48 (1.30, 1.69); moving from low to high P[M.sub.2:5] areas increased risk of all 14 diseases: infections [1.37 (1.19, 1.58)], blood diseases [1.57 (1.34, 1.84)], endocrine diseases [1.77 (1.50, 2.09)], mental and behavioral disorders [1.93 (1.68, 2.21)], nervous system diseases [1.51 (1.32, 1.74)], ocular diseases [1.76 (1.56, 1.98)], ear disorders [1.58 (1.35, 1.86)], circulatory diseases [1.59 (1.42, 1.78)], respiratory diseases [1.51 (1.33, 1.72)], digestive diseases [1.74 (1.58, 1.92)], skin diseases [1.39 (1.22, 1.58)], musculoskeletal diseases [1.62 (1.45, 1.81)], genitourinary diseases [1.54 (1.36, 1.74)] and cancer [1.42 (1.24, 1.63)]. We observed similar associations for P[M.sub.10] and S[O.sub.2] with 14 diseases (but not with all-cause mortality); increases in N[O.sub.2] and N[O.sub.x] were positively associated with 14 diseases and all-cause mortality. CONCLUSIONS: This study supports potential associations between ambient air pollution exposure and morbidity as well as mortality. Findings also emphasize the importance of maintaining consistently low levels of air pollution to protect the public's health. https://doi.org/10.1289/EHP14367, Introduction Ambient air pollution plays an important role in increasing morbidity and mortality worldwide. (1,2) It was estimated that ~6:7 million deaths were attributable to air pollution exposure in 2019. [...]

Background: Estrogens play a critical role in parturition, and poly- and perfluoroalkyl substances (PFAS), which have estrogenic effects, have been associated with preterm birth. However, the impact of estrogens on the association between PFAS and preterm birth is unknown. Objective: The objective of this study is to investigate if estrogens modified the association between PFAS and preterm birth, using a nested case-control study design. Methods: A total of 371 preterm births and 508 controls were selected from a birth cohort study in China between 2016 and 2018. Perfluorobutanoic acid (PFBA), perfluorohexanesulfonic acid (PFHxS) and its branched isomer, perfluorooctanoic acid (PFOA), perfluorooctanesulfonic acid (PFOS) and its branched isomer, and perfluorononanoic acid (PFNA) were quantified in maternal serum (mean gestational age of 32 wk). Estradiol and estriol were quantified in cord serum. Preterm birth was defined as live delivery at Results: Overall, higher odds ratios (ORs) of preterm birth were associated with each 1 ln-unit PFAS increase: PFBA [1.20, 95% confidence interval (CI): 1.14, 1.26], PFNA (1.30, 95% CI: 1.21, 1.39), PFOA (1.98, 95% CI: 1.54, 2.55), and PFOS (1.91, 95% CI: 1.76, 2.07) and its branched isomer (1.91, 95% CI: 1.90, 1.92). We detected statistically significant interactions between cord estradiol and PFAS on preterm birth, while no mediation effects of cord estrogen were observed. The ORs of PFOS (4.29, 95% CI: 1.31, 8.25), its branched isomer (6.71, 95% CI: 1.06, 11.91), and preterm birth were greater for participants with high cord estrogen levels than for participants with low cord estrogen levels. Discussion: Our findings suggest that estrogen modified the association between maternal PFAS exposure and preterm birth. Further studies on maternal PFAS exposure and preterm birth, taking interaction effects of cord estrogens into account, are warranted. https://doi.org/10.1289/EHP11377, Introduction Poly- and perfluoroalkyl substances (PFAS) comprise more than 4,000 unique chemicals, some of which are ubiquitous in the environment. (1) Exposure to PFAS is a growing public health concern. [...]

Background: Although healthy lifestyle has been linked with a reduced risk of cardiovascular diseases (CVDs), the potential metabolic mechanism underlying this association remains unknown. Methods: We included 161,018 CVD-free participants from the UK Biobank. Elastic net regression was utilized to generate a healthy lifestyle-related metabolic signature. The Cox proportional hazards model was applied to investigate associations of lifestyle-related metabolic signature with incident CVDs, and mediation analysis was conducted to evaluate the potential mediating role of metabolic profile on the healthy lifestyle-CVD association. Mendelian randomization (MR) analysis was conducted to detect the causality. Results: During 13 years of follow-up, 17,030 participants developed incident CVDs. A healthy lifestyle-related metabolic signature comprising 123 metabolites was established, and it was inversely associated with CVDs. The hazard ratio (HR) was 0.83 (95% confidence interval [CI]: 0.81, 0.84) for CVD, 0.83 (95% CI: 0.81, 0.84) for ischemic heart disease (IHD), 0.86 (95% CI: 0.83, 0.90) for stroke, 0.86 (95% CI: 0.82, 0.89) for myocardial infarction (MI), and 0.75 (95% CI: 0.72, 0.77) for heart failure (HF) per standard deviation increase in the metabolic signature. The metabolic signature accounted for 20% of the association between healthy lifestyle score and CVD. Moreover, MR showed a potential causal association between the metabolic signature and stroke. Conclusions: Our study revealed a potential link between a healthy lifestyle, metabolic signatures, and CVD. This connection suggests that identifying an individual's metabolic status and implementing lifestyle modifications may provide novel insights into the prevention of CVD. [ABSTRACT FROM AUTHOR]

The email of the corresponding author, Hualiang Lin, was incorrectly stated and should be linhualiang@mail.sysu.edu.cn. In addition, the funding recipient was incorrectly listed as H.T.L. Funding support was awarded to [...]

Background: The associations between air pollution exposure and morbidity and mortality of cardiovascular diseases (CVDs) have been widely reported; however, evidence on such associations across different dynamic disease trajectories remain unknown. Objective: We examined whether ambient air pollution during the prehypertension (pre-HTN) stage could aggravate the progression from hypertension (HTN) to CVD, and consequent death. Methods: A total of 168,010 adults with pre-HTN (120-139 mmHg systolic blood pressure or 80-89 mmHg diastolic blood pressure) from the UK Biobank were included in this analysis. We used a multistate model to explore the associations between five air pollutants (P[M.sub.2.5], P[M.sub.2.5] absorbance, P[M.sub.10], N[O.sub.2], and N[O.sub.x]) and the risk of six disease transitions (from pre-HTN to HTN, from pre- HTN to CVD, from pre-HTN to death, from HTN to CVD, from HTN to death, and from CVD to death). Mediation analyses were further conducted to explore the role of intermediate diseases in the dynamic progression of CVDs. Results: During a median follow-up of 12 y, 13,743 (8.18%) of participants with pre-HTN developed HTN, whereas 12,825 (7.63%) and 4,467 (2.66%) directly developed CVD or died, respectively. Air pollution was positively associated with the dynamic disease progression. For example, a per-interquartile range increase of P[M.sub.2.5] was significantly associated with the hazard ratios (HRs) of 1.105 [95% confidence intervals (CI): 1.083, 1.127], 1.045 (95% CI: 1.022, 1.068), and 1.086 (95% CI: 1.047, 1.126) in the transition from pre-HTN to HTN, CVD, and death, respectively. Higher levels of air pollution were associated with increased transition probability of disease progression. Mediation analyses indicated that intermediate diseases subsequently significantly mediated air pollutant-associated risk to develop more serious disease. Conclusions: This study provides evidence that air pollution might play a role in the early stages of CVD progression. Controlling air pollution might be an effective measure to prevent CVD progression and reduce the disease burden of CVD. https://doi.org/10.1289/EHP10967, Introduction Cardiovascular diseases (CVDs), including ischemic heart disease (IHD), atrial fibrillation (AF), stroke, and heart failure (HF) and a number of other heart and blood vessel disorders, comprise the leading [...]

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of the coronavirus disease (COVID-19) pandemic, is highly contagious and can put families of healthcare professionals at risk for both symptomatic [...]