About half of the world population and more than 90% of rural households in the developing countries still use unprocessed biomass fuels (wood, dung and crop residues) as the fuels. These substances, burning in the open fire or in the simple stoves, can cause indoor air pollution and the pollutants exposure in women and children is more serious. Biomass smoke contains lots of toxic and harmful substances which may impact the health of human. This article presented a recent research progress in the indoor air pollution and health effects caused by combustion of biomass fuels in China and in the world.

With the rapid economic growth and the development of transportation in China in recent two decades, the number of motor vehicles in China keeps increasing at an annual rate of approximately 13%. The air pollution related to traffic has become the focus of attention and the air pollution pattern in some large cities in China has been shifting from the coal-burning pollution to that mainly from the traffic. The traffic pollution deteriorates the environment and has been related to an increased risk of respiratory and cardiovascular diseases in the population. The state of automobile exhaust pollution and the related health effect in the urban areas of China was discussed in the present paper.

Objective To clarify whether ethanol induced cytotoxicity of neurons was inhibited by proteasome peptidase activities. Methods A rat pheochromocytoma(PC12) was used in the present study. Cytotoxicity and proteasome peptidase activities were assessed in PC12 cells exposed to 50, 100, 150 mmol/L, 200 and 300 mmol/L ethanol. Results After 48 hours of treatment, ethanol inhibited proteasome peptidase activity in a dose-dependent manner at the concentration above 100 mmol/L. Moreover, the effect of ethanol on activities of proteasome was also in a time-dependent manner from 24 h. Cytotoxicity was still observed as ethanol concentrations increasing, started from 100 mmol/L, as assessed by MTT method. Conclusion Our results demonstrates ethanol may disturb the metabolism of protein by inhibiting proteasome peptidase activities, which is related to the toxic mechanism of ethanol on PC12 cells.

Recent studies have shown a significant relationship between ambient particulate matter and cardiovascular diseases.Results of epidemiological and experimental studies in recent years were reviewed in the present paper.The biological mechanisms of the ambient particulate matter-induced cardiovascular impacts were also discussed.

SUMMARY Traffic noise pollution problem is increasingly emerging with the rapid developmentof urban traffic. Researchers have paid close attention to the health effects of traffic noise. This review has summarized the recent research progress in the health effects of traffic noise both at home and abroad. Traffic noise can have various ad-verse health effects, and most of them are extra-auditory effects. The main aspects include that traffic noise can af-fect the cardiovascular system, which is verified by the evidence that exposure to traffic noise significantly increases the risk for cardiovascular diseases, such as high blood pressure, myocardial infarction, coronary heart disease, and so on. In addition, traffic noise can induce adverse effects on nervous system, leading to the increasing levels of anxiety, noise annoyance, and occurrence of insomnia. Furthermore, traffic noise is significantly associated with adverse pregnant outcomes, and can affect the endocrine system and digestive system. As traffic noise and traffic related air pollutants co-exist in the traffic environment, whether there are joint effects between these two factors have become areas of research focus nowadays. Although there is sufficient evidence that traffic noise has adverse health effects, inadequacies still existe. Analysis of the shortages of current studies and the prospects of the future studies are pointed out in this review.

Objective To investigate the contamination level of environmental tobacco smoke (ETS) in the public places and workplaces in Dongcheng district of Beijing and identify the influencing factors for ETS exposure. Methods The contamination level of ETS in 14 public places and workplaces of Dongcheng district were monitored with passive sampler of vapor-phase nicotine during Apr.-Feb.,2004. Results Nicotine was detected from all monitor sites at the 14 locations. The lowest air nicotine concentration was detected in no smoking places and the highest one was detected in non-regulation places. There were many factors which were found to influence the indoor air nicotine concentration,including legislation,the number of smokers and the room space,etc. The most significant factor was found to be the numbers of smokers. Conclusion Exposure to ETS in the pubic places and workplaces has become a major pubic and occupational health issue at present.

Objective To investigate the effects of PM2.5 on gap junctional intercellular communication (GJIC) between rat cardiomyocytes. Methods Primary cultured cardiomyocytes were prepared from 1-day-old Sprague-Dawley rats and exposed to PM2.5(1,10,100 ?g/ml)for 24 hours. The GJIC between cardiomyocytes was detected by the scrape loading dye transfer assay. The distribution and density of connexin43(Cx43) in the cells was detected by indirect immunofluorescence and the expression of Cx43 was detected by western blotting. Results The gap junctional intercellular communication between cardiomyocytes was significantly inhibited by PM2.5 in a dose-dependent manner. The fluorescence density of Cx43 was significantly decreased in PM2.5-treated cells,and the expression of Cx43 was also slightly decreased. Conclusion PM2.5 can inhibit GJIC between cardiomyocytes,which may be mediated by the decreased expression and aberrant distribution of Cx43 in PM2.5-treated cells.

Objective To study the acute effects of PM2.5 on the heart rhythm of spontaneously hypertensive rats(SHR)and the mechanism.Methods Twenty-eight male spontaneously hypertensive rats(SHR)were randomly divided into four groups.PM2.5 was administered by intratracheal instillation at the doses of 0 mg/kg,7.5 mg/kg,15 mg/kg and 30 mg/kg respectively.ECGs were monitored at 30 min,1 h and 24 h later.Results The numbers of the rats with arrhythmia in all groups increased at 30 min after treatment.At 1 h after treatment,in control group the rats recovered,but in PM2.5 groups abnormal ECGs was still showed.However,ECGs of all groups became normal 24 h later.As shown by laser scanning confocal microscope(LSCM),the expression of Cx43 in the heart tissue of rats in 15 mg/kg and 30 mg/kg groups significantly decreased compared with the control group.There was no significant change in content of MDA and SOD in the heart tissue of PM2.5 treated rats.Conclusion PM2.5 exposure through inhalation may induce arrhythmia in SHR rats and the downregulated expression of Cx43 may play an important role in the pathogenesis.

Objective To understand the ambient PM2.5 component and the toxicity to primary cultured myocardial cells of neonatal rats. Methods Primary myocardial cells cultures were prepared from 1-day-old Sprague-Dawley rats and treated with PM2.5 suspension and its organic and water-soluble extracts at various concentrations for 24 h. The cellular viability was measured with MTT methods, and the beat of myocardial cells was observed and counted under inverted microscope. Results PM2.5 suspension and its organic and water-soluble extracts increased the viability of myocardial cells at the concentrations below 10.0 ?g/ml, but above this, they could significantly decrease the viability of myocardial cells with a dose-dependent manner. The toxicity of organic extract of PM2.5 was significantly higher than that of water-soluble extract. PM2.5 suspension and its organic and water-soluble extracts also dose-dependently inhibited the beat frequencies of myocardial cells. Conclusion PM2.5 and its extracts show a hormesis effect on the cultured myocardial cells in the case of the cellular viability is taken as the response parameter. PM2.5 and its extracts can inhibit the beat of myocardial cells.

Objective:To investigate the effects of nanoscale titanium dioxide(Nano-TiO2) on gap junctional intercellular communication(GJIC) between human lung fibroblasts.Methods: Human lung fibroblasts were exposed to two different sizes Nano-TiO2(25 nm and 80 nm) for 24 hours at the concentrations of 0,10,20,40 and 80 mg/L,respectively.The GJIC between cells was measured by using fluorescence redistribution after photobleaching(FRAP) assay.Results: The results showed that GJIC between cells was significantly inhibited both by 25 nm and 80 nm Nano-TiO2 in a dose-dependent manner.The fluorescence recovery rate was 20.81%?1.93% in control group,7.26%?0.91%(P