The association between air pollutants and morbidity for diabetes and liver diseases modified by sexes, ages, and seasons in Tianjin, China

Tong, Ling; Li, Kai; Zhou, Qixing

doi:10.1007/s11356-014-3432-4

Cited by 37 publications

(21 citation statements)

References 30 publications

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“…Our findings are consistent with previous studies suggesting glycemic effects of air pollution (Basile and Bloch, 2012;Coogan et al, 2012;Eze et al, 2014;Goldberg et al, 2006;Kan et al, 2004;Kramer et al, 2010;Raaschou-Nielsen et al, 2013;Tong et al, 2015). Several cohort studies have shown that exposure to air pollution was associated with DM.…”

Section: Discussionsupporting

confidence: 93%

“…Many studies have reported that the mortality/morbidity risks related to air pollution are more significant in the elderly than the young (Chen et al, 2012a;Kan et al, 2008). This may because the elderly experienced greater exposure to the outdoor air pollution environment than the young owing to work necessities (Tong et al, 2015). Also, the elderly are more sensitive than younger people to the air pollution because of physiology.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, more and more attention has been paid to the potential impacts of exposure to air pollution on increased incidence, prevalence, and mortality of DM (Basile and Bloch, 2012;Bhatnagar, 2009;Brook et al, 2013a;Coogan et al, 2012;Eze et al, 2014;Goldberg et al, 2000;Goldberg et al, 2006;Kan et al, 2004;Kramer et al, 2010;Raaschou-Nielsen et al, 2013;Sun et al, 2009;Tong et al, 2015;Zanobetti and Schwartz, 2001;Zanobetti and Schwartz, 2002). A meta-analysis showed that there were significant associations between long-term exposure to PM 2.5 , PM 10 and NO 2 , and DM morbidity and mortality in developed countries (USA, Canada and European countries) .…”

Section: Introductionmentioning

confidence: 99%

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Air pollution and fasting blood glucose: A longitudinal study in China

Chen

Zhou

et al. 2016

Science of The Total Environment

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Limited studies have examined the associations between air pollutants [particles with diameters of 10 μm or less (PM10), sulphur dioxide (SO2), and nitrogen dioxide (NO2)] and fasting blood glucose (FBG). We collected data for 27,685 participants who were followed during 2006 and 2008. Generalized Estimating Equation models were used to examine the effects of air pollutants on FBG while controlling for potential confounders. We found that increased exposure to NO2, SO2 and PM10 was significantly associated with increased FBG levels in single pollutant models (p<0.001). For exposure to 4 days' average of concentrations, a 100 μg/m(3) increase in SO2, NO2, and PM10 was associated with 0.17 mmol/L (95% CI: 0.15-0.19), 0.53 mmol/L (95% CI: 0.42-0.65), and 0.11 mmol/L (95% CI: 0.07-0.15) increase in FBG, respectively. In the multi-pollutant models, the effects of SO2 were enhanced, while the effects of NO2 and PM10 were alleviated. The effects of air pollutants on FBG were stronger in female, elderly, and overweight people than in male, young and underweight people. In conclusion, the findings suggest that air pollution increases the levels of FBG. Vulnerable people should pay more attention on highly polluted days to prevent air pollution-related health issues.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Air pollution and fasting blood glucose: A longitudinal study in China

Chen

Zhou

et al. 2016

Science of The Total Environment

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“…Evidence abounds that levels of GSH in the body decreases naturally with age [ 7 ]. Both stressful life style and some artificial components of foods are the popular culprits [ 8 ]. Due to some theoretical benefits of maintaining antioxidant defenses status, several approaches to increase systemic and/or tissue-specific glutathione concentrations have been of scientific interests.…”

Section: Introductionmentioning

confidence: 99%

Toxicological evaluation of therapeutic and supra-therapeutic doses of Cellgevity® on reproductive function and biochemical indices in Wistar rats

Awodele

Badru

Busari

et al. 2018

BMC Pharmacol Toxicol

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BackgroundThe misconception about dietary supplements being safe has led many into the in-patient wards. Cellgevity® (CGV) is a Max International premiere antioxidant supplement formula used by a large population. This study evaluated the effects of therapeutic and supra-therapeutic doses of CGV on reproductive function and biochemical indices in Wistar rats.MethodsSeventy-two Wistar rats weighing 130 ± 15.8 g were grouped into two categories (male or female) of six rats per group. Control group received distilled water (10 ml/kg). Others received therapeutic (14.3 mg/kg or 28.6 mg/kg) and supra-therapeutic CGV doses (1000, 2000 or 3000 mg/kg) body weight per oral respectively.ResultsAfter 60 days, supra-therapeutic doses of CGV reduced sperm motility (p < 0.05) by 31.8%, 31.3% and 34.5% respectively and increased (p < 0.05) abnormality in sperms by 200%, 241% and 141.3% respectively. CGV altered male (luteinizing, follicle stimulating hormones and testosterone) and female reproductive hormones (luteinizing, follicle stimulating hormones estrogen and progesterone) respectively. Therapeutic doses of CGV elevated reduced glutathione, superoxide dismutase, catalase and glutathione S-transferase, although, this was exceeded by supra-therapeutic doses and more in females than male rats. Supra-therapeutic dose (3000 mg/kg CGV) decreased body weight in both male and female rats by 50% (F(1.5, 30) = 1.2, p = 0.041) and 62.7% (F(2.1, 30) = 0.38, p = 0.038) respectively in treated rats. Supratherapeutic (3000 mg/kg) dose of CGV increased (p < 0.05) creatinine level by 99.1% while serum total protein was reduced (p < 0.05) by 60.1% (2000 mg/kg) and 57.2% (3000 mg/kg) respectively in male animals. In Female rats, supra-therapeutic doses of CGV elevated creatinine levels by 72.2% (1000 mg/kg), 60.2% (2000 mg/kg) and 124.8% (3000 mg/kg) respectively and 3000 mg/kg produces elevated serum low density lipoprotein by 34.6% in treated rats. Serum cholesterol, triglycerides, albumin, alkaline phosphatase were unaltered by CGV dosing. Histology shows seminiferous tubules with reduced spermatogenic cells. Also, female rat kidney revealed acute tubular necrosis at highest dose used in this study.ConclusionOverall, these data suggest that pro-oxidant potential of the supra-therapeutic CGV doses is evident. Hence, it is necessary that its administration be done with caution using appropriate doses.

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“…Epidemiological investigations reveal that SO 2 pollution not only increase the risk of many respiratory diseases (Guo et al, 2014;Liu et al, 2014) but is also associated with circulatory system diseases (Amancio and Nascimento, 2012), such as heart disease (Li et al, 2015;Dong et al, 2015), congenital malformation (Farhi et al, 2014) and liver disease (Tong et al, 2015). Increasing evidence suggests that SO 2 inhalation is also linked to neurotoxicity and aggravates the risk for hospitalization and mortality of many brain disorders, including ischemic stroke (Amancio and Nascimento, 2014), cerebral hemorrhage (Ye et al, 2009), epilepsy (Cakmak et al, 2010), neurodevelopmental impairment and cognitive deficit (Lin et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Endocannabinoid 2-arachidonoylglycerol protects inflammatory insults from sulfur dioxide inhalation via cannabinoid receptors in the brain

Chen

Guo

et al. 2017

Journal of Environmental Sciences

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Sulfur dioxide (SO) pollution in the atmospheric environment causes brain inflammatory insult and inflammatory-related microvasculature dysfunction. However, there are currently no effective medications targeting the harmful outcomes from chemical inhalation. Endocannabinoids (eCBs) are involved in neuronal protection against inflammation-induced neuronal injury. The 2-arachidonoylglycerol (2-AG), the most abundant eCBs and a full agonist for cannabinoid receptors (CB1 and CB2), is also capable of suppressing proinflammatory stimuli and improving microvasculature dysfunction. Here, we indicated that endogenous 2-AG protected against neuroinflammation in response to SO inhalation by inhibiting the activation of microglia and astrocytes and attenuating the overexpression of inflammatory cytokines, including tumor necrosis factor alpha (TNF-a), interleukin (IL)-1β, and inducible nitric oxide synthase (iNOS). In addition, endogenous 2-AG prevented cerebral vasculature dysfunction following SO inhalation by inhibiting endothelin 1 (ET-1), vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) expression, elevating endothelial nitric oxide synthase (eNOS) level, and restoring the imbalance between thromboxane A2 (TXA2) and prostaglandin I2 (PGI2). In addition, the action of endogenous 2-AG on the suppression of inflammatory insult and inflammatory-related microvasculature dysfunction appeared to be mainly mediated by CB1 and CB2 receptors. Our results provided a mechanistic basis for the development of new therapeutic approaches for protecting brain injuries from SO inhalation.

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The association between air pollutants and morbidity for diabetes and liver diseases modified by sexes, ages, and seasons in Tianjin, China

Cited by 37 publications

References 30 publications

Air pollution and fasting blood glucose: A longitudinal study in China

Air pollution and fasting blood glucose: A longitudinal study in China

Toxicological evaluation of therapeutic and supra-therapeutic doses of Cellgevity® on reproductive function and biochemical indices in Wistar rats

Endocannabinoid 2-arachidonoylglycerol protects inflammatory insults from sulfur dioxide inhalation via cannabinoid receptors in the brain

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