Excessive exposure to light at night (LAN) has become a serious public health concern. However, little is known about the impact of indoor LAN exposure on blood pressure, particularly among young adults. We aimed to investigate the effects of bedroom individual-level LAN exposure in real-world environment on blood pressure and hypertension among vulnerable young adults, and to evaluate the possible buffering effect of physical activity. In this cross-sectional study, a total of 400 healthy young adults aged 16–22 years were included. Bedroom LAN exposure was recorded at 1-min intervals for two consecutive nights using a TES-1339 R illuminance meter. Blood pressure was measured three times (8–11 a.m. in the physical examination day) in the seated position using an Omron HEM-7121 digital sphygmomanometer. A wrist-worn triaxial accelerometer (ActiGraph GT3X-BT) was used to assess physical activity for seven consecutive days. Each 1 lx increase of bedroom LAN intensity was associated with 0.55 mmHg-increase in SBP (95% CI: 0.15, 0.95), 0.30 mmHg-increase in DBP (95% CI: 0.06, 0.54), and 0.38 mmHg-increase in MAP (95% CI: 0.12, 0.65). Higher levels of LAN exposure were associated with increased risk of hypertension (LAN ≥ 3lx vs. LAN < 3lx: OR = 3.30, 95%CI = 1.19–9.19; LAN ≥ 5lx vs. LAN < 5lx: OR = 3.87, 95%CI = 1.37–10.98). However, these detrimental effects of bedroom LAN exposure on blood pressure and hypertension were not observed among young adults with high MVPA (≥2 h/day) level. MVPA can alleviate negative effects of bedroom LAN exposure on blood pressure and hypertension. Maintaining bedroom settings darkness at night may be an important strategy for reducing the risk of hypertension. Furthermore, for individuals living with high levels of indoor LAN exposure, regular physical activity may be a good option for preventing cardiovascular disease and hypertension.

The association of co-exposure to polycyclic aromatic hydrocarbons (PAHs) and phthalates (PAEs) with blood cell-based inflammatory biomarkers is largely unknown. We conducted a panel study of 144 children aged 4–12 years, with up to 3 repeated visits across 3 seasons. For each visit, we collected the first-morning urine for 4 consecutive days and fasting blood on the day of physical examination. We developed a gas chromatography/tandem mass spectrometry method to detect the metabolites of 10 PAHs (OH-PAHs) and 10 PAEs (mPAEs) in urine samples. We employed linear mixed-effects models to evaluate the individual associations of each OH-PAH and mPAE with blood cell-based inflammatory biomarkers over different lag times. Bayesian kernel machine regression (BKMR) and quantile g-computation were used to evaluate the overall associations of OH-PAHs and mPAEs mixtures with blood cell-based inflammatory biomarkers. After multiple adjustments, we found positive associations of summed hydroxylphenanthrene (∑OHPHE), summed OH-PAHs, and mono-n-butyl phthalate with inflammatory biomarkers such as neutrophil count, neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, and the systemic immune-inflammation index (SII) at lag 0 (the day of physical examination). Each 1% increase in ∑OHPHE was related to a 0.18% (95% confidence interval: 0.10%, 0.25%) increase in SII, which was the strongest among the above associations. The results of BKMR and quantile g-computation suggested that co-exposure to PAHs and PAEs mixture was associated with an elevated white blood cell count, neutrophil count, neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, and SII, to which ∑OHPHE and 1-hydroxypyrene (1-OHPYR) might be the major contributors. In addition, gender and age modified the associations of ∑OHPHE and 1-OHPYR with inflammatory biomarkers, where girls and younger children were more susceptible. In conclusion, co-exposure to PAHs and PAEs was associated with elevated inflammation in children, in which ∑OHPHE and 1-OHPYR might play important roles.

Evidence is available about the associations of phthalates or their metabolites with blood lipids, however, the mixture effects of multiple phthalate metabolites on blood lipid traits remain largely unknown. In this pilot study, 106 individuals at three age groups of <18, 18- and ≥60 years were recruited from the residents (n = 1240) who were randomly selected from two communities in Wuhan city, China. The participants completed the questionnaire survey and physical examination as well as provided urine samples in the winter of 2014 and the summer of 2015. We measured urinary levels of nine phthalate metabolites using a high-performance liquid chromatography-tandem mass spectrometry. We estimated the associations of individual phthalate metabolite with blood lipid traits by linear mixed effect (LME) models, and assessed the overall association of the mixture of nine phthalate metabolites with blood lipid traits using Bayesian kernel machine regression (BKMR) models. LME models revealed the negative association of urinary mono-2-ethylhexyl phthalate (MEHP) with total cholesterol (TC) as well as of urinary mono-benzyl phthalate or urinary MEHP with low density lipoprotein cholesterol (LDL-C). BKMR models revealed the negative overall association of the mixture of nine phthalate metabolites with TC or LDL-C, and DEHP metabolites (especially MEHP) had a greater contribution to TC or LDL-C levels than non-DEHP metabolites. The findings indicated the negative overall association of the mixture of nine phthalate metabolites with TC or LDL-C. Among nine phthalate metabolites, MEHP was the most important component for the changes of TC or LDL-C levels, implying that phthalates exposure may disrupt lipid metabolism in the body.

Metabolic syndrome is an important risk factor for non-communicable diseases, particularly type 2 diabetes, coronary heart disease, and stroke. Long-term exposure to greenspace could be protective of metabolic syndrome, but evidence for such an association is lacking. Accordingly, we investigated the association between long-term exposure to greenspace and risk of metabolic syndrome.The present longitudinal study was based on data from four clinical examinations between 1997 and 2013 in 6076 participants of the Whitehall II study, UK (aged 45–69 years at baseline). Long-term exposure to greenspace was assessed by satellite-based indices of greenspace including Normalized Difference Vegetation Index (NDVI) and Vegetation Continuous Field (VCF) averaged across buffers of 500 and 1000 m surrounding the participants’ residential location at each follow-up. The ascertainment of metabolic syndrome was based on the World Health Organization (WHO) definition. Hazard ratios for metabolic syndrome were estimated using Cox proportional hazards regression models, controlling for age, sex, ethnicity, lifestyle factors, and socioeconomic status.Higher residential surrounding greenspace was associated with lower risk of metabolic syndrome. An interquartile range increase in NDVI and VCF in the 500 m buffer was associated with 13% (95% confidence interval (CI): 1%, 23%) and 14% (95% CI: 5%, 22%) lower risk of metabolic syndrome, respectively. Greater exposure to greenspace was also associated with each individual component of metabolic syndrome, including a lower risk of high levels of fasting glucose, large waist circumference, high triglyceride levels, low HDL cholesterol, and hypertension. The association between residential surrounding greenspace and metabolic syndrome may have been mediated by physical activity and exposure to air pollution.The findings of the present study suggest that middle-aged and older adults living in greener neighbourhoods are at lower risk of metabolic syndrome than those living in neighbourhoods with less greenspace.

PM₂.₅ (particulate matter ≤2.5 μm in aerodynamic diameter) is a major urban air pollutant worldwide. Its effects on the respiratory system of the susceptible population have been less characterized. This study aimed to estimate the association of short-term PM₂.₅ exposure with respiratory outcomes of the retired adults, and to examine whether these associations were stronger among the subjects with GSTT-null genotype. 32 healthy subjects (55–77 years) were recruited for five follow-up examinations. Ambient concentrations of PM₂.₅ were monitored consecutively for 7 days prior to physical examination. Pulmonary outcomes including forced vital capacity (FVC), forced expiratory volume in 1 s (FEV₁), peak expiratory flow (PEF), and fractional exhaled nitric oxide (FeNO), and nasal fluid concentrations of 8-epi-prostaglandin F2 alpha (8-epi-PGF2α), tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8) and IL-1β were measured. A linear mixed-effect model was introduced to evaluate the associations of PM₂.₅ concentrations with respiratory outcomes. Additionally, GSTT1 genotype-based stratification was performed to characterize modification on PM₂.₅-related respiratory outcomes. We found that a 10 μg/m³ increase in PM₂.₅ was associated with decreases of 0.52 L (95% confidence interval [CI]: -1.04, -0.002), 0.64 L (95% CI: -1.13, -0.16), 0.1 (95% CI: -0.23, 0.04) and 2.87 L/s (95% CI: -5.09, -0.64) in FVC, FEV₁, FEV₁/FVC ratio and PEF at lag 2, respectively. Meanwhile, marked increases of 80.82% (95% CI: 5.13%, 156.50%) in IL-8, 77.14% (95% CI: 1.88%, 152.40%) in IL-1β and 67.87% (95% CI: 14.85%, 120.88%) in 8-epi-PGF2α were observed as PM₂.₅ concentration increased by 10 μg/m³ at lag 2. Notably, PM₂.₅-associated decreases in FVC and PEF and increase in FeNO were stronger among the subjects with GSTT1-null genotype. In summary, short-term exposure to PM₂.₅ is associated with nasal inflammation, oxidative stress and lung function reduction in the retired subjects. Lung function reduction and inflammation are stronger among the subjects with GSTT1-null genotype.

Previous studies indicated that exposure to air pollution was associated with the progress of atherosclerosis, but evidence is very limited in China and even in the world. This study aims to assess the associations of long-term exposures to air pollution and greenness with the occurrence of carotid plaque. Participants of this cohort study were urban residents and office workers who visited Hebei General Hospital for routine physical examination annually from September 2016 through to December 2018. Eligible participants were people diagnosed the absence of carotid plaque clinically at their first hospital visit and were followed up at their second or third hospital visit. Exposure to particulate matter with aerodynamic diameter less than 2.5 μm (PM₂.₅), nitrogen dioxide (NO₂) and ozone (O₃) were estimated using an inverse distance weighted (IDW) method. The level of greenness was assessed using the Normalized Difference Vegetation Index (NDVI) and Enhanced Vegetation Index (EVI). The associations were evaluated using Cox proportional hazards regression models. Among 4,137 participants, 575 showed the occurrence of carotid plaque during the follow-up period. After controlling for potential confounders, the hazard ratios (HRs) and 95% confidence intervals (95%CIs) of carotid plaque associated with per interquartile range (IQR) increase in PM₂.₅, NO₂, and O₃ were 1.78 (1.55, 2.03), 1.32 (1.14, 1.53) and 1.99 (1.71, 2.31), respectively. Increased EVI and NDVI were significantly associated with lower risk of carotid plaque [HR (and 95%CI): 0.84 (0.77, 0.93) and 0.87 (0.80, 0.94)]. PM₂.₅ significantly mediated 80.47% or 93.00% of the estimated association between EVI or NDVI and carotid plaque. In light of the significant associations between air pollution, greenness and carotid plaque in this study, continued efforts are needed to curb air pollution and plan more green space considering their effects on vascular disease.

Inflammation may play an important role in the association between exposure to polycyclic aromatic hydrocarbons (PAHs) and atherosclerotic cardiovascular disease (ASCVD) risk. However, the underlying mechanisms remain unclear.To investigate the association of PAHs exposure with ASCVD risk and effects of mean platelet volume (MPV) or Club cell secretory protein (CC16) on the association.A total of 2022 subjects (689 men and 1333 women) were drawn from the baseline Wuhan residents of the Wuhan-Zhuhai Cohort study. Data on demography and the physical examination were obtained from each participant. Urinary monohydroxy PAH metabolites (OH-PAHs) levels were measured by a gas chromatography-mass spectrometry. We estimated the association between each OH-PAHs and the 10-year ASCVD risk or coronary heart disease (CHD) risk using logistic regression models, and further analyze the mediating effect of MPV or plasma CC16 on the association by using structural equation modeling.The results of multiple logistic regression models showed that some OH-PAHs were positively associated with ASCVD risk but not CHD risk, including 2-hydroxyfluoren (β = 1.761; 95% CI: 1.194–2.597), 9-hydroxyfluoren (β = 1.470; 95% CI: 1.139–1.898), 1-hydroxyphenanthrene (β = 1.480; 95% CI: 1.008–2.175) and ΣOH-PAHs levels (β = 1.699; 95% CI: 1.151–2.507). The analysis of structural equation modeling shows that increased MPV and increased plasma CC16 levels contributed 13.6% and 15.1%, respectively, to the association between PAHs exposure and the 10-year ASCVD risk (p < 0.05).Exposure to PAHs may increase the risk of atherosclerosis, which was partially mediated by MPV or CC16.

Cleaning products are mixtures of many chemical ingredients that are known to contain sensitizers, disinfectants, and fragrances, as well as strong airway irritants which associated with lower respiratory tract and asthma symptoms. The aim of this study is to assess the prevalence and possible risk factors of occupational asthma and its effect on quality of life among workers in detergent and cleaning products industries in El Asher men Ramadan city. This cross-sectional study was conducted on 780 workers. All participants were personally interviewed at their workplaces and were subjected to a questionnaire regarding sociodemographic, work characteristics and asthma symptoms, clinical examination, chest X-ray, spirometer, and bronchodilator test. The prevalence of occupational asthma among the studied workers was 35.4%. Multivariate logistic regression analysis revealed that female gender [odds ratio 1.397; 95% CI 1.09–1.96], manually working participants [odds ratio 3.067; 95% CI 1.72–5.46], and history of atopy [odds ratio 1.596; 95% CI 1.09–2.33] were risk factors for development of occupational asthma. The total mean score of asthma-specific quality of life was significantly lower in asthmatic (5.10 ± 0.49) than non-asthmatic workers (5.89 ± 0.46) (P < 0.01) indicating impairment of quality of life among asthmatic group. Workers in detergent and cleaning products industry are at higher risk for developing occupational asthma that adversely affects their general health and quality of life.

The decision of intensive care unit (ICU) admission in acute pesticide poisoning is often challenging, especially in developing countries with limited resources. This study was conducted to compare the efficacy of the Acute Physiology and Chronic Health Evaluation II (APACHE II), Modified Early Warning Score (MEWS), and Poisoning Severity Score (PSS) in predicting ICU admission and mortality of acute pesticide-poisoned patients. This prospective cohort study included all patients admitted to Tanta University Poison Control Center with acute pesticide poisoning from the start of March 2018 to the end of March 2019. Patient data, including demographic and toxicological data, clinical examination, laboratory investigation, and score values, were collected on admission. Out of 337 acute pesticide-poisoned patients, 30.5% were admitted to the ICU, including those poisoned with aluminum phosphide (ALP) (81.5%) and organophosphates (OP) (18.5%). Most non-survivors (86.6%) were ALP poisoning. The PSS had the best discriminatory power in predicting ICU admission and mortality, followed by APACHE II and MEWS. However, no significant difference in predicting ICU admission of OP-poisoned patients was detected between the scores. Additionally, no significant difference in mortality prediction of ALP-poisoned patients was found between the PSS and APACHE II. The PSS, APACHE II, and MEWS are good discriminators for outcome prediction of acute pesticide poisoning on admission. Although the PSS showed the best performance, MEWS was simpler, more feasible, and practicable in predicting ICU admission of OP-poisoned patients. Moreover, the APACHE II has better sensitivity for mortality prediction of ALP-poisoned patients.

Our aim was to clarify the main factors associated with lung function and to analyze the correlation between fine particulate matter (PM₂.₅) and lung function in a rural Chinese population. We analyzed data of 5195 participants in the China Northwest Natural Population Cohort: Ningxia Project who were ≥ 30 years old. They were recruited from 2018 to 2019, underwent spirometry during the physical examination, and completed a self-report questionnaire. A satellite-based spatiotemporal model was used to estimate the 2-year average PM₂.₅ exposure based on participants’ home addresses. A generalized linear mixed model was used to test the relationship between PM₂.₅ concentration and lung function. Sex, age, exposure to cooking oil fumes, and occupational exposure were negatively correlated (P < 0.05) with forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV₁). Educational status, economic level, tea consumption, and alcohol consumption were positively correlated (P < 0.05) with FVC and FEV₁. The adjusted results of each model revealed that FVC and FEV₁ decreased with increased exposure to PM₂.₅. There was a strong negative correlation between a PM₂.₅ concentration of 35.66 μg/m³ and FVC, FEV1, and FEV1/FVC, with unadjusted hazard ratios of − 0.06 (95% confidence interval, − 0.10 to − 0.01), − 0.13 (− 0.17 to − 0.10), and − 22.10 (− 24.62 to − 19.26), respectively. In conclusion, long-term exposure to high concentrations of ambient PM₂.₅ is related to reduce lung function among people in rural areas in northwestern China.