Fresh fruit, dried fruit, raw vegetables, and cooked vegetables consumption associated with progression trajectory of type 2 diabetes: a multi-state analysis of a prospective cohort.

PURPOSE: To examine the effects of fresh fruit, dried fruit, raw vegetables, and cooked vegetables on type 2 diabetes (T2D) progression trajectory. METHODS: We included 429,886 participants in the UK Biobank who were free of diabetes and diabetes complications at baseline. Food groups were determined using a validated food frequency questionnaire. Outcomes were T2D incidence, complications, and mortality. Multi-state model was used to analyze the effects of food groups on T2D progression. RESULTS: During a follow-up of 12.6 years, 10,333 incident T2D cases were identified, of whom, 3961 (38.3%) developed T2D complications and 1169 (29.5%) died. We found that impacts of four food groups on T2D progression varied depending on disease stage. For example, compared to participants who ate less than one piece of dried fruit per day, the hazard ratios and 95% confidence intervals for those who ate ≥ 2 pieces of dried fruit per day were 0.82 (0.77, 0.87), 0.88 (0.85, 0.92), and 0.86 (0.78, 0.95) for transitions from diabetes-free state to incident T2D, from diabetes-free state to total death, and from incident T2D to T2D complications, respectively. Higher intake of fresh fruit was significantly associated with lower risk of disease progression from diabetes-free state to all-cause death. Higher intake of raw and cooked vegetables was significantly associated with lower risks of disease progression from diabetes-free state to incident T2D and to total death. CONCLUSIONS: These findings indicate that higher intake of fresh fruit, dried fruit, raw vegetables, and cooked vegetables could be beneficial for primary and secondary prevention of T2D.

Empirical dynamic modeling of the association between ambient PM2.5 and under-five mortality across 2851 counties in Mainland China, 1999-2012.

BACKGROUND: Ambient fine particulate matter (PM2.5) pollution has been associated with mortality from various diseases, however, its association with under-five mortality rate (U5MR) has remained largely unknown. METHODS: Based on the U5MR data across 2851 counties in Mainland China from 1999 to 2012, we employed approximate Bayesian latent Gaussian models to assess the association between ambient PM2.5 and U5MR at the county level for the whole nation and sub-regions. GDP growth rate, normalized difference vegetation index (NDVI), temperature, and night-time light were included as covariates using a smoothing function. We further implemented an empirical dynamic model (EDM) to explore the potential causal relationship between PM2.5 and U5MR. RESULTS: We observed a declining trend in U5MR in most counties throughout the study period. Spatial heterogeneity in U5MR was observed. Nationwide analysis suggested that each 10 µg/m3 increase in annual concentration of PM2.5 was associated with an increase of 1.2 (95% CI: 1.0 - 1.3) per 1000 live births in U5MR. Regional analyses showed that the strongest positive association was located in the Northeastern part of China [1.8 (95% CI: 1.4 - 2.1)]. The EDM showed a significant causal association between PM2.5 and U5MR, with an embedding dimension of 5 and 7, and nonlinear values θ of 4 and 6, respectively. CONCLUSION: China exhibited a downward trend in U5MR from 1999 to 2012, with spatial heterogeneity observed across the country. Our analysis reveals a positive association between PM2.5 and U5MR, which may support a causal relationship.

Air Pollution Metabolomic Signatures and Chronic Respiratory Diseases Risk: A Longitudinal Study.

BACKGROUND: Although evidence has documented the associations of ambient air pollution with chronic respiratory diseases (CRDs) and lung function, the underlying metabolic mechanisms remain largely unclear. RESEARCH QUESTION: How does the metabolomic signature for air pollution relate to CRD risk, respiratory symptoms, and lung function? STUDY DESIGN AND METHODS: We retrieved 171,132 participants free of COPD and asthma at baseline from the UK Biobank, who had data on air pollution and metabolomics. Exposures to air pollutants (particulate matter with diameter ≤ 2.5 µm [PM2.5], particulate matter with a diameter ≤ 10 µm, nitrogen oxide [NOX], and NO2) were assessed for 4 years before baseline considering residential address histories. We used 10-fold cross-validation elastic net regression to identify air pollution-associated metabolites. Multivariable Cox models were used to assess the associations between metabolomic signatures and CRD risk. Mediation and pathway analysis were conducted to explore the metabolic mechanism underlying the associations. RESULTS: During a median follow-up of 12.51 years, 8,951 and 5,980 incident COPD and asthma cases were recorded. In multivariable Cox regressions, air pollution was positively associated with CRD risk (eg, hazard ratio per interquartile range increment in PM2.5, 1.09; 95% CI, 1.06-1.13). We identified 103, 86, 85, and 90 metabolites in response to PM2.5, particulate matter with a diameter ≤ 10 µm, NOX, and NO2 exposure, respectively. The metabolomic signatures showed significant associations with CRD risk (hazard ratio per SD increment in PM2.5 metabolomic signature, 1.11; 95% CI, 1.09-1.14). Mediation analysis showed that peripheral inflammatory and erythrocyte-related markers mediated the effects of metabolomic signatures on CRD risk. We identified 14 and 12 perturbed metabolic pathways (energy metabolism and amino acid metabolism pathways, etc) for PM2.5 and NOX metabolomic signatures. INTERPRETATION: Our study identifies metabolomic signatures for air pollution exposure. The metabolomic signatures showed significant associations with CRD risk, and inflammatory- and erythrocyte-related markers partly mediated the metabolomic signatures-CRD links.

Short-Term Ambient Air Pollution and Urticaria in Guangzhou, China: Estimating the Association and Population Attributable Fraction.

Limited evidence is available regarding the association between acute exposure to ambient air pollutants and the risk of urticaria, even though the skin is an organ with direct contact with the external environment. This study utilized generalized additive models to investigate the association between particulate matter with an aerodynamic diameter smaller than 10 µm (PM10) and 2.5 µm (PM2.5), nitrogen dioxide (NO2) and sulfur dioxide (SO2), and daily outpatient visits for urticaria in Guangzhou, China from 2013 to 2017. We also estimated the attributable fraction of urticaria outpatient visits due to air pollution. A total of 216,648 outpatient visits due to urticaria occurred during the study period. All air pollutants were significantly associated with an increased excess risk of urticaria. Each 10 µg/m3 increase in PM2.5, PM10, NO2, and SO2 was associated with an increase of 1.23% (95% CI: 0.42%, 2.06%), 0.88% (95% CI: 0.28%, 1.49%), 3.09% (95% CI: 2.16%, 4.03%), and 2.82% (95% CI: 0.93%, 4.74%) in hospital visits for urticaria at lag05, respectively. It was estimated that 3.77% (95% CI: 1.26%, 6.38%), 1.91% (95% CI: 0.60%, 3.26%), 6.36% (95% CI: 4.38%, 8.41%), and 0.08% (95% CI: 0.03%, 0.14%) of urticaria outpatient visits were attributable to PM2.5, PM10, NO2, and SO2 using the World Health Organization's air quality guideline as the reference. Relatively stronger associations were observed during the cold season. This study indicates that short-term air pollution may play a significant role in outpatient visits for urticaria, and that such relationships could be modified by season.