BackgroundEnvironmental pollutants such as polycyclic aromatic hydrocarbons (PAHs), lead, and mercury are released by combustion of coal and other fossil fuels.ObjectivesIn the present study we evaluated the association between prenatal exposure to these pollutants and child development measured by the Gesell Developmental Schedules at 2 years of age.MethodsThe study was conducted in Tongliang, Chongqing, China, where a seasonally operated coal-fired power plant was the major source of ambient PAHs and also contributed lead and mercury to the air. In a cohort of nonsmoking women and their newborns enrolled between March 2002 and June 2002, we measured levels of PAH–DNA adducts, lead, and mercury in umbilical cord blood. PAH–DNA adducts (specifically benzo[a]pyrene adducts) provided a biologically relevant measure of PAH exposure. We also obtained developmental quotients (DQs) in motor, adaptive, language, and social areas.ResultsDecrements in one or more DQs were significantly associated with cord blood levels of PAH–DNA adducts and lead, but not mercury. Increased adduct levels were associated with decreased motor area DQ (p = 0.043), language area DQ (p = 0.059), and average DQ (p = 0.047) after adjusting for cord lead level, environmental tobacco smoke, sex, gestational age, and maternal education. In the same model, high cord blood lead level was significantly associated with decreased social area DQ (p = 0.009) and average DQ (p = 0.038).ConclusionThe findings indicate that exposure to pollutants from the power plant adversely affected the development of children living in Tongliang; these findings have implications for environmental health policy.

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BackgroundCoal burning provides 70% of the energy for China’s industry and power, but releases large quantities of polycyclic aromatic hydrocarbons (PAHs) and other pollutants. PAHs are reproductive and developmental toxicants, mutagens, and carcinogens.ObjectiveWe evaluated the benefit to neurobehavioral development from the closure of a coal-fired power plant that was the major local source of ambient PAHs.MethodsThe research was conducted in Tongliang, Chongqing, China, where a coal-fired power plant operated seasonally before it was shut down in May 2004. Two identical prospective cohort studies enrolled nonsmoking women and their newborns in 2002 (before shutdown) and 2005 (after shutdown). Prenatal PAH exposure was measured by PAH–DNA adducts (benzo[a]pyrene–DNA) in umbilical cord blood. Child development was assessed by the Gesell Developmental Schedules at 2 years of age. Prenatal exposure to other neurotoxicants and potential confounders (including lead, mercury, and environmental tobacco smoke) was measured. We compared the cohorts regarding the association between PAH–DNA adduct levels and neurodevelopmental outcomes.ResultsSignificant associations previously seen in 2002 between elevated adducts and decreased motor area developmental quotient (DQ) (p = 0.043) and average DQ (p = 0.047) were not observed in the 2005 cohort (p = 0.546 and p = 0.146). However, the direction of the relationship did not change.ConclusionThe findings indicate that neurobehavioral development in Tongliang children benefited by elimination of PAH exposure from the coal-burning plant, consistent with the significant reduction in PAH–DNA adducts in cord blood of children in the 2005 cohort. The results have implications for children’s environmental health in China and elsewhere.

Berberine is known to improve glucose and lipid metabolism disorders, but the mechanism is still under investigation. In this paper, we explored the effects of berberine on the weight, glucose levels, lipid metabolism, and serum insulin of KKAy mice and investigated its possible glucose and lipid-regulating mechanism. We randomly divided KKAy mice into two groups: berberine group (treated with 250 mg/kg/d berberine) and control group. Fasting blood glucose (FBG), weight, total cholesterol (TC), triglyceride (TG), high-density lipoprotein-cholesterol (HDL-c), low-density lipoprotein-cholesterol (LDL-c), and fasting serum insulin were measured in both groups. The oral glucose tolerance test (OGTT) was performed. RT2 PCR array gene expression analysis was performed using skeletal muscle of KKAy mice. Our data demonstrated that berberine significantly decreased FBG, area under the curve (AUC), fasting serum insulin (FINS), homeostasis model assessment insulin resistance (HOMA-IR) index, TC, and TG, compared with those of control group. RT2 profiler PCR array analysis showed that berberine upregulated the expression of glucose transporter 4 (GLUT4), mitogen-activated protein kinase 14 (MAPK14), MAPK8(c-jun N-terminal kinase, JNK), peroxisome proliferator-activated receptor α (PPARα), uncoupling protein 2 (UCP2), and hepatic nuclear factor 4α(HNF4α), whereas it downregulated the expression of PPARγ, CCAAT/enhancer-binding protein (CEBP), PPARγ coactivator 1α(PGC 1α), and resistin. These results suggest that berberine moderates glucose and lipid metabolism through a multipathway mechanism that includes AMP-activated protein kinase-(AMPK-) p38 MAPK-GLUT4, JNK pathway, and PPARα pathway.

Temporomandibular disorders (TMD) are a group of clinical problems affecting temporomandibular joint (TMJ), myofascial muscles and other related structures. Splint therapy is the most commonly used approach to treatment of TMD, but its effectiveness is remains unclear. We therefore conducted a meta-analysis to evaluate the effectiveness of splint therapy for TMD in adults. The electronic databases PubMed, EMBASE, Cochrane Library, and ClinicalTrials.gov were searched for reports published up to March 31, 2016. Thirteen eligible studies involving 538 patients were identified. The results indicated that splint therapy increased maximal mouth opening (MMO) for patients with a MMO <45mm and reduced pain intensity measured using the visual analogue scale (VAS) for patients with TMD without specific description (TMDSD). Splint therapy also reduced the frequency of painful episodes for patients with TMJ clicking. No publication bias was observed, as determined with Egger's test for all outcomes. On the basis of this evidence, we recommend the use of splints for the treatment and control of TMD in adults.

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Siloxanes are used in a wide variety of personal-care and other consumer products. Although there is clearly a potential for contamination of indoor dust with siloxanes, reports of occurrence of siloxanes in indoor dust were not available, prior to the present study. Here, we have determined the concentrations and profiles of four cyclic siloxanes, octamethylcyclotetrasiloxane (D(4)), decamethylcyclopentasiloxane (D(5)), dodecamethylcyclohexasiloxane (D(6)), and tetradecamethylcycloheptasiloxane (D(7)), as well as 11 linear siloxanes, from L(4)-L(14), in 100 dust samples collected in China. Cyclic and linear siloxanes were found in all dust samples, with the linear siloxanes L(9)-L(14) being the predominant compounds. Concentrations of total siloxanes in dust ranged from 21.5 to 21,000 (mean: 1540 +/- 2850) ng g(-1). The highest concentration of the individual linear siloxanes, L(9)-L(14), ranged between 2680 and 6170 ng g(-1). Concentrations of total linear siloxanes (TLS) were 1-2 orders of magnitude higher than concentrations of total cyclic siloxanes (TCS), in all indoor dust samples. Siloxane concentrations in dust were associated with the number of electrical/electronic appliances, number of occupants, and smokers living in the house. Based on the measured siloxane concentrations and on estimated daily ingestion rates of dust by toddlers and adults, we calculated the daily intake of siloxanes. For adults, daily exposure to total siloxanes, based on an average dust intake rate and median exposure concentration, was calculated to be 15.9 ng day(-1); the corresponding value for toddlers was 32.8 ng d(-1).

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