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Numerous cohort studies have reported the association of long-term exposure to particulate matter

Several studies have researched the short-term effect of sulfur dioxide (SO2) exposure on hypertension. However, no evidence has provided the relationship between long-term high pollution exposure of SO2 and morbidity of hypertension in cohort studies in China. This retrospective cohort study aimed to evaluate this association. We used Cox proportional hazards regression models to examine the hazard ratios (HR) for hypertension risks from 1998 to 2009 associated with accumulative exposure of air SO2 among adults in northern China. Annual average concentrations of sulfur dioxide (SO2) were obtained from 15 local environmental monitoring centers. Hypertension was identified according to self-reported diagnostic time and treatment for hypertension with anti-hypertensive medication. Among 37,386 participants, 2619 new cases of hypertension were identified during 426,334 person-years. In the fully adjusted model, HR and 95% confidence interval (CI) of hypertension incidence for each 10 μg/m3 increase in SO2 were 1.176 (1.163 and 1.189). Results from stratified analyses suggested that effects of SO2 on hypertension morbidity were more pronounced in participants

Evidence is still limited for the role of long-term PM2.5 exposure in cerebrovascular diseases among residents in high pollution regions. The study is aimed to investigate the long-term effects of PM2.5 exposure on stroke mortality, and further explore the effect modification of temperature variation on the PM2.5-mortality association in northern China. Based on a cohort data with an average follow-up of 9.8 years among 38,435 urban adults, high-resolution estimates of PM2.5 derived from a satellite-based model were assigned to each participant. A Cox regression model with time-varying exposures and strata of geographic regions was employed to assess the risks of stroke mortality associated with PM2.5, after adjusting for individual risk factors. The cross-product term of PM2.5 exposure and annual temperature range was further added into the regression model to test whether the long-term temperature variation would modify the association of PM2.5 with stroke mortality. Among the study participants, the annual mean level of PM2.5 concentration was 66.3 μg/m3 ranging from 39.0 μg/m3 to 100.6 μg/m3. For each 10 μg/m3 increment in PM2.5, the hazard ratio (HR) was 1.31 (95% CI: 1.04–1.65) for stroke mortality after multivariable adjustment. In addition, the HRs of PM2.5 decreased gradually as the increase of annual temperature range with the HRs of 1.95 (95% CI: 1.36–2.81), 1.53 (95% CI: 1.06–2.22), and 1.11 (95% CI: 0.75–1.63) in the low, middle, and high group of annual temperature range, respectively. The findings provided further evidence of long-term PM2.5 exposure on stroke mortality in high-exposure settings such as northern China, and also highlighted the view that assessing the adverse health effects of air pollution might not ignore the role of temperature variations in the context of climate change.

Background Ambient air pollution has recently been related to type 2 diabetes mellitus (T2DM), a disease that has caused an economic and health burden worldwide. Evidence of an association between air pollution and T2DM was reported in the United States and Europe. However, few studies have focused on the association with high levels of air pollutants in a developing country. Objectives We conducted a 12-year cohort study to assess the incidence and mortality of T2DM associated with long-term exposure to PM10, SO2, and NO2. Methods A retrospective cohort with participants from four cities in northern China was conducted to assess mortality and incidence of T2DM from 1998 to 2009. Incidence of T2DM was self-reported, and incident intake of an antidiabetic drug or injection of insulin simultaneously and mortality of T2DM was obtained from a family member and double checked against death certificates provided from the local center for disease control and prevention. Individual pollution exposures were the mean concentrations of pollutants estimated from the local environmental monitoring centers over the survival years. Hazard ratios (HRs) were estimated using Cox regression models after adjusting for potential confounding factors. Results A total of 39 054 participants were recruited into the mortality cohort, among which 59 subjects died from T2DM; 38 529 participants were analyzed in the incidence cohort, and 1213 developed new cases of T2DM. For each 10 μg/m3 increase in PM10, SO2, and NO2, the adjusted HRs and 95% confidence interval (CI) for diabetic incidence were 1.831 (1.778, 1.886), 1.287 (1.256, 1.318), and 1.472 (1.419, 1.528), respectively. Similar results can be observed in the analysis of diabetic mortality with HRs (95% CI) up to 2.260 (1.732, 2.950), 1.130 (1.042, 1.225), and 1.525 (1.280, 1.816), respectively. Conclusions Our results suggested that long-term exposure to high levels of PM10, SO2, and NO2 increase risk of incident and mortality of T2DM in China.

The health effects of metals and benzene exposure have been extensively investigated; however, information on the impact of chronic environmental metal and benzene exposure on human urinary metabolome is limited. In this study, a total of 566 participants, including 352 elderly and 214 children, were split into the “exposed” and “control” groups. The urine samples of all the participants were collected and stored at − 80 °C until analysis. The urinary levels of 17 metals and S-phenylmercapturic acid (S-PMA) were determined by the ICP–MS and LC–MS/MS methods to comprehensively assess the personal metal and benzene exposure levels, respectively. Then, the individual levels of metal and benzene exposure were correlated to the metabolic consequences of ambient pollutant exposure, which were previously observed in our metabolomics study. As a result, multiple metals, including Cd, Co, Cr, Cu, Fe, Hg, Li, Mo, Ni, Pb, Se, and Zn, exhibited a significant linear dose–dependent association with one or more urinary metabolites, including two amino acids (pyroglutamic acid and 3-methylhistidine), three organic acids (azelaic acid, decenedioic acid, and hydroxytetradecanedioic acid), ten medium-chainacylcarnitines (heptenedioylcarnitine, octenedioylcarnitine, nonenedioylcarnitine, decenedioylglucuronide, 3-hydroxydecanoylcarnitine, dodecanedioylcarnitine, nonanoylcarnitine, decadienylcarnitine, hydroxydodecenoylcarnitine, dodecadienylcarnitine, and dodecenoylcarnitine), and one glucuronide conjugate (decenedioylglucuronide). These observations indicate that the increased environmental metal exposure has caused various oxidative stress-related effects, including the depletion of antioxidants, accelerated muscle proteolysis, elevated activity of UGTs, increased lipid peroxidation, and the disorder of mitochondrial lipid metabolism among exposed children and the elderly. The current study provides new insights into the biological effects induced by metal exposure in the environment.

The toxicities of polycyclic aromatic hydrocarbons (PAHs) have been extensively explored due to their carcinogenic and mutagenic potency; however, little is known about the metabolic responses to chronic environmental PAH exposure among the general population. In the present study, 566 healthy volunteers were dichotomized into exposed and control groups to investigate PAH-induced perturbations in the metabolic profiles. Nine urine PAH metabolites were measured by a sensitive LC-MS/MS method to comprehensively evaluate the PAH exposure level of each individual, and the metabolic profiles were characterized via a LC-MS-based metabolomic approach. PAH exposure was correlated to its metabolic outcomes by linear and logistic regression analyses. Metabolites related to amino acid, purine, lipid, and glucuronic acid metabolism were significantly changed in the exposed group. 1-Hydroxyphenanthrene and dodecadienylcarnitine have potential as sensitive and reliable biomarkers for PAH exposure and its metabolic outcomes, respectively, in the general population. These findings generally support the hypothesis that environmental PAH exposure causes oxidative stress-related effects in humans. The current study provides new insight into the early molecular events induced by PAH exposure in the actual environment.

Epidemiologic studies have demonstrated that long-term exposure to relatively low levels of particulate air pollution is associated with adverse cardiovascular outcomes in Europe and North America. However, few studies have assessed the association with high level air pollutants. We aimed to assess the cardiovascular effects of long-term exposure to high level concentrations of inhalable particulate and to identify the characteristics of the Chinese population that are susceptible to the health effects. A retrospective cohort, containing 39,054 subjects from four cities in northern China, was followed for mortality of all cause and specific cardiovascular diseases from 1998 to 2009. Information on concentrations of PM10 (particulate matter

Objective The aim of this study was to establish the concentration–response relationships between the levels of SO2 and PM10 and the daily numbers of pediatric outpatient visits and to estimate ben...

Objective: To explore and descript the association of air pollution with outpatient visits in a hospital Taiyuan during 2013 haze episode. Methods: Data of outpatient visits were collected in a com...

OBJECTIVE: To determine the shape of concentration-response function for air pollution related children’s hospital admissions across a high and wide range of air pollution in Yangquan, China (PM10:...

Background Localized birth weight references for gestational age serve as an essential tool in accurate evaluation of atypical birth outcomes (e.g. small for gestational age) in clinical diagnosis and region-specific epidemiological studies. Such standards are currently not available in Mainland China. Aims To construct up-to-date, sex- and parity-specific birth weight references based on 231,937 births in Taiyuan, China during years 2005–2011. Study design Population-based, cross-sectional. Subjects Hospital-registered, healthy infants with births dated between 11/01/2005 and 12/31/2011 within Taiyuan area. Outcome measures Birth weight in grams, and gestational age in complete weeks were calculated using a combination of last-menstrual-date-based estimation and ultrasound examination. Results Separate birth weight references are constructed for male and female infants born from primiparous and multiparous mothers. Male infants are found to weigh more than female infants in later gestational ages (appr. weeks 33–42), and infants born to multiparous mother are found to weigh more than infants born to primiparous mothers in later gestational ages (appr. weeks 36–42). Conclusions The Taiyuan birth weight reference curves display similar trends of growth as reference curves from other countries worldwide (Netherlands, Scotland, Australia, Canada, Hong Kong, Korea and Kuwait). However, growth of birth weight for Taiyuan infants tends to be slower compared to European and North American infants regardless of gender, but similar to infants from other Asian countries.