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Background: Unraveling gene-environment interaction can provide a novel insight into early disease prevention. Nevertheless, current understanding of the interplay between genetic predisposition and air pollution in relation to myocardial infarction (MI) risk remains limited. Furthermore, the potential long-term influence of air pollutants on MI incidence risk warrants more conclusive evidence in a community population., Objective: We investigated interactions between genetic predisposition and exposure to air pollutants on MI incidence., Methods: This study incorporated a sample of 456,354 UK Biobank participants and annual mean air pollution ( PM 2.5 , PM 10 , NO 2 , and NO x ) from the UK Department for Environment, Food and Rural Affairs (2006-2021). The Cox proportional hazards model was employed to explore MI incidence after chronic air pollutants exposure. By quantifying genetic risk through the calculation of polygenic risk score (PRS), this study further examined the interactions between genetic risk and exposure to air pollutants in the development of MI on both additive and multiplicative scales., Results: Among 456,354 participants, 9,114 incident MI events were observed during a median follow-up of 12.08 y. Chronic exposure to air pollutants was linked with an increased risk of MI occurrence. Specifically, the hazard ratios (per interquartile range) were 1.12 (95% CI: 1.10, 1.13) for PM 2.5 , 1.20 (95% CI: 1.19, 1.22) for PM 10 , 1.13 (95% CI: 1.12, 1.15) for NO 2 , and 1.12 (95% CI: 1.11, 1.13) for NO x . In terms of the joint effects, participants with high PRS and high level of air pollution exposure exhibited the greatest risk of MI among all study participants ( ∼ 255 % to 324%). Remarkably, both multiplicative and additive interactions were detected in the ambient air pollutants exposure and genetic risk on the incidence of MI., Discussion: There were interactions between exposure to ambient air pollutants and genetic susceptibility on the risk of MI onset. Moreover, the joint effects of these two exposures were greater than the effect of each factor alone. https://doi.org/10.1289/EHP14291.

Background: Benzene affects human health through environmental exposure in addition to occupational contact. However, few studies have examined the associations between long-term exposure to low concentrations of ambient benzene and mortality risks in nonoccupational settings. Methods: This prospective cohort study consists of 393,042 participants without stroke, myocardial infarction, or cancer at baseline from the UK Biobank. Annual average concentrations of benzene for each year during follow-up were measured using air dispersion models. The main outcomes were all-cause mortality and mortality from specific causes. Cox proportional-hazards models with time-varying exposure measurements were used to estimate the hazard ratios and 95% confidence intervals (CIs) for mortality risks. Restricted cubic spline models were used to estimate exposure-response relationships. Measurements and Main Results: With each interquartile range increase in the average annual concentration of benzene, the adjusted hazard ratios of mortality risk from all causes, cardiovascular disease, cancer, and respiratory disease were 1.26 (95% CI, 1.24-1.27), 1.24 (95% CI, 1.21-1.28), 1.27 (95% CI, 1.25-1.29), and 1.25 (95% CI, 1.20-1.30), respectively. The monotonically increasing exposure-response curves showed no threshold and plateau within the observed concentration range. Furthermore, the effect of benzene exposure on mortality persisted across different subgroups and was somewhat stronger in younger and White people ( P for interaction < 0.05). Conclusions: Long-term exposure to low concentrations of ambient benzene significantly increases mortality risk in the general population. Ambient benzene represents a potential threat to public health, and further investigations are needed to support timely pollution regulation and health protection.

Evidences on the association between exposure to air pollution and liver enzymes was scarce in low pollution area. We aimed to investigate the association between air pollution and liver enzyme levels and further explore whether alcohol intake influence this association. This cross-sectional study included 425,773 participants aged 37 to 73 years from the UK Biobank. Land Use Regression was applied to assess levels of PM 2.5 , PM 10 , NO 2 , and NOx. Levels of liver enzymes including AST, ALT, GGT, and ALP were determined by enzymatic rate method. Long-term low-level exposure to PM 2.5 (per 5-μg/m 3 increase) was significantly associated with AST (0.596% increase, 95% CI, 0.414 to 0.778%), ALT (0.311% increase, 0.031 to 0.593%), and GGT (1.552% increase, 1.172 to 1.933%); The results were similar for PM 10 ; NO X and NO 2 were only significantly correlated with AST and GGT Significant modification effects by alcohol consumption were found (P-interaction < 0.05). The effects of pollutants on AST, ALT, and GGT levels gradually increased along with the weekly alcohol drinking frequency. In conclusion, long-term low-level air pollutants exposure was associated with elevated liver enzyme levels. And alcohol intake may exacerbate the effect of air pollution on liver enzymes., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Background: Short-term exposure to air pollution has been linked to pneumonia risk. However, evidence on the long-term effects of air pollution on pneumonia morbidity is scarce and inconsistent. We investigated the associations of long-term air pollutant exposure with pneumonia and explored the potential interactions with smoking., Research Question: Is long-term exposure to ambient air pollution associated with the risk of pneumonia, and does smoking modify the associations?, Study Design and Methods: We analyzed data in 445,473 participants without pneumonia within 1 year before baseline from the UK Biobank. Annual average concentrations of particulate matter (particulate matter with a diameter < 2.5 μm [PM 2.5 ] and particulate matter with a diameter < 10 μm [PM 10 ]), nitrogen dioxide (NO 2 ), and nitrogen oxides (NO x ) were estimated using land-use regression models. Cox proportional hazards models were used to assess the associations between air pollutants and pneumonia incidence. Potential interactions between air pollution and smoking were examined on both additive and multiplicative scales., Results: The hazard ratios of pneumonia for each interquartile range increase in PM 2.5 , PM 10 , NO 2 , and NO x concentrations were 1.06 (95% CI, 1.04-1.08), 1.10 (95% CI, 1.08-1.12), 1.12 (95% CI, 1.10-1.15), and 1.06 (95% CI, 1.04-1.07), respectively. There were significant additive and multiplicative interactions between air pollution and smoking. Compared with individuals who had never smoked with low air pollution exposure, individuals who had ever smoked with high air pollution exposure had the highest pneumonia risk (PM 2.5 : hazard ratio [HR], 1.78; 95% CI, 1.67-1.90; PM 10 : HR, 1.94; 95% CI, 1.82-2.06; NO 2 : HR, 2.06; 95% CI, 1.93-2.21; NO x : HR, 1.88; 95% CI, 1.76-2.00). The associations between air pollutants and pneumonia risk persisted in participants exposed to air pollutants concentrations meeting the European Union limits., Interpretation: Long-term exposure to air pollutants was associated with an increased risk of pneumonia, especially in individuals who smoke., (Copyright © 2023 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.)

Background and Aims: The adverse effects of air pollutants on the risk of most cardiovascular diseases (CVDs) are well-established, but the risk of CVDs such as deep vein thrombosis, pulmonary embolism, or aortic valve stenosis have been underappreciated, especially in the diabetic population. This study aimed to evaluate associations between long-term air pollutants exposure and the risk of incident CVDs among participants with diabetes., Methods: This study included 27,827 participants with baseline diabetes from the UK Biobank. We then estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for CVDs associated with chronic air pollutant exposure in the diabetic population by fitting the Cox proportional hazards model. Moreover, we investigated the cardiovascular effects of air pollutants at concentrations below WHO guideline limits., Results: After multivariable adjustment, long-term NO 2 and NO x exposures were positively associated with the development of 8 and 6 types of CVDs in participants with diabetes, respectively. In term of particulate matters, the effect estimates ranged from 1.51 (1.13, 2.03) (coronary artery disease) to 4.65 (2.73, 7.92) (peripheral arterial disease) per 10 μg/m 3 increase in PM 2.5 . Whereas, the effect estimates ranged from 1.15 (1.04, 1.27) (arterial hypertension) to 2.28 (1.40, 3.69) (pulmonary embolism) per 10 μg/m 3 increase in PM 10 . In addition, our study discovered that for most of the cardiovascular events (8 of 9), the deleterious effects of air pollutants persisted even when participants were exposed to air pollutants concentrations below WHO guideline limits., Conclusions: Long-term exposure to ambient NO 2 , NO x , PM 2.5 , and PM 10 , either at normal or low level, increased risk of various cardiovascular outcomes in the diabetic population., 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 © 2023 Elsevier B.V. All rights reserved.)

Background: Evidence linking air pollution to major depressive disorder (MDD) remains sparse and results are heterogeneous. In addition, the evidence about the interaction and joint associations of genetic risk and lifestyle with air pollution on incident MDD risk remains unclear. We aimed to examine the association of various air pollutants with the risk of incident MDD and assessed whether genetic susceptibility and lifestyle influence the associations., Methods: This population-based prospective cohort study analyzed data collected between March 2006 and October 2010 from 354,897 participants aged 37 to 73 years from the UK Biobank. Annual average concentrations of PM 2.5 , PM 10 , NO 2 , and NO x were estimated using a Land Use Regression model. A lifestyle score was determined based on a combination of smoking, alcohol drinking, physical activity, television viewing time, sleep duration, and diet. A polygenic risk score (PRS) was defined using 17 MDD-associated genetic loci., Results: During a median follow-up of 9.7 years (3,427,084 person-years), 14,710 incident MDD events were ascertained. PM 2.5 (HR: 1.16, 95% CI: 1.07-1.26; per 5 μg/m 3 ) and NO x (HR: 1.02, 95% CI: 1.01-1.05; per 20 μg/m 3 ) were associated with increased risk of MDD. There was a significant interaction between the genetic susceptibility and air pollution for MDD (P-interaction < 0.05). Compared with participants with low genetic risk and low air pollution, those with high genetic risk and high PM 2.5 exposure had the highest risk of incident MDD (PM 2.5 : HR: 1.34, 95% CI: 1.23-1.46). We also observed an interaction between PM 2.5 exposure and unhealthy lifestyle (P-interaction < 0.05). Participants with the least healthy lifestyle and high air pollution exposures had the highest MDD risk when compared to those with the most healthy lifestyle and low air pollution (PM 2.5 : HR: 2.22, 95% CI: 1.92-2.58; PM 10 : HR: 2.09, 95% CI: 1.78-2.45; NO 2 : HR: 2.11, 95% CI: 1.82-2.46; NO x : HR: 2.28, 95% CI: 1.97-2.64)., Conclusions: Long-term exposure to air pollution is associated with MDD risk. Identifying individuals with high genetic risk and developing healthy lifestyle for reducing the harm of air pollution to public mental health., (© 2023. The Author(s).)

Background: Air pollutants are considered as non-negligible risk factors of idiopathic pulmonary fibrosis (IPF). However, the relationship between long-term air pollution and the incidence of IPF is unknown. Our objective was to explore the associations of air pollutants with IPF risk and further assess the modification effect of genetic susceptibility., Methods: We used land-use regression model estimated concentrations of nitrogen dioxide (NO 2 ), nitrogen oxides (NO x ) and particulate matter (fine particulate matter with diameter <2.5 μm (PM 2.5 ) and particulate matter with diameter <10 μm (PM 10 )). The polygenic risk score (PRS) was constructed using 13 independent single nucleotide polymorphisms. Cox proportional hazard models were used to evaluate the associations of air pollutants with IPF risk and further investigate the modification effect of genetic susceptibility. Additionally, absolute risk was calculated., Results: Among 433 738 participants from the UK Biobank, the incidence of IPF was 27.45 per 100 000 person-years during a median follow-up of 11.78 years. The adjusted hazard ratios of IPF for each interquartile range increase in NO 2 , NO x and PM 2.5 were 1.11 (95% CI 1.03-1.19), 1.07 (95% CI 1.01-1.13) and 1.09 (95% CI 1.02-1.17), respectively. PM 2.5 had the highest population attribution risk, followed by NO x and NO 2 . There were additive interactions between NO 2 , NO x and PM 2.5 and genetic susceptibility. Participants with a high PRS and high air pollution had the highest risk of incident IPF compared with those with a low PRS and low air pollution (adjusted hazard ratio: NO 2 3.94 (95% CI 2.77-5.60), NO x 3.08 (95% CI 2.21-4.27), PM 2.5 3.65 (95% CI 2.60-5.13) and PM 10 3.23 (95% CI 2.32-4.50))., Conclusion: Long-term exposures to air pollutants may elevate the risk of incident IPF. There are additive effects of air pollutants and genetic susceptibility on IPF risk., Competing Interests: Conflict of interest: The authors disclose that there are no potential competing financial interests or personal relationships that could affect the work reported in this article., (Copyright ©The authors 2023. For reproduction rights and permissions contact permissions@ersnet.org.)

Background: The effect of long-term exposure to air pollution on the development of chronic obstructive pulmonary disease (COPD) is still controversial, and the role of the interactions of air pollution with genetic risk and lifestyle in COPD risk is unclear., Methods: We included 452762 participants derived from the UK Biobank. Annual concentrations of air pollutions, including particle matter (PM 2.5 , PM 10 ), nitrogen oxides (NO x ), and nitrogen dioxide (NO 2 ), were assessed using land-use regression model. We applied Cox proportional hazard model to evaluate the associations between air pollution and COPD risk. In addition, we constructed a polygenic risk score and a lifestyle score, and assessed whether genetic susceptibility and lifestyle modified the effect of air pollution on the COPD risk., Findings: Each interquartile range (IQR) increase in annual concentrations of PM 2.5 , PM 10 , NO x , and NO 2 was associated with 1.17 (95% CI: 1.15,1.19), 1.05 (95% CI: 1.03,1.06), 1.13 (95% CI: 1.11,1.14), and 1.19 (95% CI: 1.16,1.21) times the risk of COPD, respectively. We observed an additive interaction between PM 2.5 and genetic risk (P- interact =0.095), and a negative interaction between PM 2.5 and lifestyle (P- interact =0.062). The HRs for each IQR increase in PM 2.5 were 1.21, (95% CI: 1.16-1.25) and 1.24, (95% CI: 1.21-1.26) in individuals with healthy and unfavourable lifestyle, respectively; and 1.16, (95% CI: 1.13-1.19) and 1.19, (95% CI: 1.16-1.22) in those with low genetic risk and high genetic risk, respectively. Participants with high air pollution exposure, high genetic risk and unfavourable lifestyle showed the highest risk of COPD., Interpretation: Long-term exposure to air pollution was associated with increased risk of COPD, especially in those with high genetic risk and unfavourable lifestyle., Funding: None., Competing Interests: Declaration of interests None., (Copyright © 2022 The Authors. Published by Elsevier B.V. All rights reserved.)

Both ambient particulate matter (PM) and decrease of greenness have been suggested as risk factors for high blood pressure (HBP) in children and adolescents. But most evidence were from cross-sectional studies with limited data from prospective cohorts. In this cohort study, we included 588,004 children and adolescents aged 7 to 18 years without HBP from 2005 to 2018 in Beijing (240,081) and Zhongshan (347,923) city of China. The cumulative incidence of HBP was 32.04%, and incidence rate was 14.86 per 100 person-year. After adjustment for confounders, the ten-unit increase in PM 1 , PM 2.5 , and PM 10 exposure was significantly associated with 43%, 70%, and 43%- higher risks of HBP, respectively, but the 0.1-unit increase in NDVI exposure was significantly associated with a 25% lower risk of HBP. The HRs of PM 1 on the HBP risk were 1.486 and 1.150 in the low and the high-level of greenness, and they were 2.635 and 2.507 for PM 2.5 , and for PM 10 1.367 and 1.702 in the two groups. The attributable fraction (AFs) of PM 1 , PM 2.5 , and PM 10 on HBP incidents were 13.74%, 40.08%, and 15.47% in the low-level of greenness, which simultaneously was higher than those in the high-level of greenness (AF = 4.62%, 17.28%, and 9.96%). The exposure to higher ambient PM air pollution and lower greenness around schools were associated with a higher risk of HBP in children and adolescents, but higher greenness alleviated the adverse effects of ambient PM 1 and PM 2.5 on the HBP risks. Our findings highlighted a synergic strategy in preventing childhood HBP by decreasing air pollution reduction and improving greenness concurrently., 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 © 2021 Elsevier B.V. All rights reserved.)

Objective: The present study aims to investigate the association between PM 2.5 exposure and major depressive disorder, and to examine whether vitamin D and physical activity could attenuate the impact of PM 2.5 on major depressive disorder., Methods: 39168 elderly adults (age≥60 years) who had valid estimates on exposure of PM 2.5 in 2010 and data on major depressive disorder were extracted from the UK Biobank. Major depressive disorder was assessed by lifetime experience of mild, moderate, and severe major depression with validated instruments. Logistic regression models were used to estimate the association between PM 2.5 exposure and major depressive disorder., Results: A total of 9079 participants had major depressive disorder, with a prevalence of 23.2%. The odds ratio (OR) of major depressive disorder was 1.096 (1.023, 1.175) for participants in the highest quartile compared with the lowest quartile of PM 2.5 . The correlation of PM 2.5 with major depressive disorder generally increased with the decreasing levels of vitamin D. For instance, in participants with the highest quartile of PM 2.5 , the corresponding ORs were 1.141 (0.951, 1.369), 1.232 (1.027, 1.478), 1.286 (1.072, 1.543), and 1.390 (1.159, 1.667) for those who had adequate, desirable, insufficient, and deficient levels of vitamin D, respectively. Additionally, significant modification effects of physical activity on the relationship between PM 2.5 and major depressive disorder were also observed., Conclusions: Our study suggests that high levels of vitamin D and physical activity may attenuate the relationship between PM 2.5 and major depressive disorder among elderly adults., (Copyright © 2021 Elsevier B.V. All rights reserved.)