Mercury is emitted to the atmosphere from various natural and anthropogenic sources, and degrades with difficulty in the environment. Mercury exists as various species, mainly elemental (Hg0) and divalent (Hg2+) mercury depending on its oxidation states in air and water. Mercury emitted to the atmosphere can be deposited into aqueous environments by wet and dry depositions, and some can be re-emitted into the atmosphere. The deposited mercury species, mainly Hg2+, can react with various organic compounds in water and sediment by biotic reactions mediated by sulfur-reducing bacteria, and abiotic reactions mediated by sunlight photolysis, resulting in conversion into organic mercury such as methylmercury (MeHg). MeHg can be bioaccumulated through the food web in the ecosystem, finally exposing humans who consume fish. For a better understanding of how humans are exposed to mercury in the environment, this review paper summarizes the mechanisms of emission, fate and transport, speciation chemistry, bioaccumulation, levels of contamination in environmental media, and finally exposure assessment of humans.
Air Pollutants/chemistry/metabolism ; *Environmental Exposure ; Environmental Remediation ; Food Chain ; Humans ; Mercury/chemistry/*metabolism ; Methylmercury Compounds/chemistry/metabolism ; Photolysis ; Sulfur-Reducing Bacteria/metabolism ; Water Pollutants, Chemical/metabolism

BACKGROUND: Wood is a valuable material for interiors, and the psychophysiological relaxation effects of volatile organic compounds (VOCs) from wood chips and essential oils have been reported. However, few studies have identified the odors in full-scale wooden environment, and also, differences in gender have not been clarified. In this study, we aimed to confirm the effects of VOCs emitted from interior wood walls in both human male and female participants. METHODS: We used Japanese cedar timber and analyzed VOCs in the experimental rooms with and without Japanese cedar timber by gas chromatography-mass spectrometry (GC-MS). The physiological effects were measured using neuroendocrinological and immunological parameters in saliva. A questionnaire was used to evaluate the subjective responses to each odor in the experimental rooms. RESULTS: The main compound emitted from Japanese cedar timber was δ-cadinene, and the total volume of VOCs in the wood condition (presence of VOCs emitted from Japanese cedar) was 282.4 (μg/m). Significant differences between genders in salivary parameters were shown that there were decreases of α-amylase in wood condition and increases of cortisol in the control (absence of VOCs) condition in female participants compared to male participants. The results demonstrated that VOCs in the experimental room with Japanese cedar timber tend to suppress the activation of the sympathetic nervous activity and non-VOCs of Japanese cedar in the control room increase cortisol in female participants. CONCLUSIONS These results suggest that an indoor environment with wood interior materials has the potential to be useful for health management, especially women's health.
Adult ; Air Pollutants ; analysis ; Air Pollution, Indoor ; adverse effects ; analysis ; Cryptomeria ; chemistry ; Female ; Gas Chromatography-Mass Spectrometry ; Humans ; Hydrocortisone ; metabolism ; Male ; Saliva ; chemistry ; Salivary alpha-Amylases ; metabolism ; Sesquiterpenes ; analysis ; Sex Factors ; Volatile Organic Compounds ; adverse effects ; Wood ; chemistry ; Young Adult

OBJECTIVETo evaluate the effect of white rot fungus Phanerochaete chrysosporium on removal of gaseous chlorobenzene.

METHODSFungal mycelium mixed with a liquid medium was placed into airtight bottles. A certain amount of chlorobenzene was injected into the headspace of the bottles under different conditions. At a certain interval, the concentrations in the headspace were analyzed to evaluate the degradation of chlorobenzene by P. chrysosporium.

RESULTSThe degradation effects of P. chrysosporium on chlorobenzene under different conditions were investigated. The difference in the optimum temperature for the growth of the fungi and chlorobenzene degradation was observed. The data indicated that a lower temperature (28 degrees C) would promote the degradation of chlorobenzene than the optimum temperature for the growth of the fungi (37 degrees C). A low nitrogen source concentration (30 mg N/L) had a better effect on degrading chlorobenzene than a high nitrogen source concentration (higher than 100 mg N/L). A high initial concentration (over 1100 mg/m3) of chlorobenzene showed an inhibiting effect on degradation by P. chrysosporium. A maximum removal efficiency of 95% was achieved at the initial concentration of 550 mg/m3.

CONCLUSIONP. chrysosporium has a rather good ability to remove gaseous chlorobenzene. A low nitrogen source concentration and a low temperature promote the removal of chlorobenzene by P. chrysosporium. However, a high initial chlorobenzene concentration can inhibit chlorobenzene degradation.

Air Pollutants ; metabolism ; Biodegradation, Environmental ; Chlorobenzenes ; metabolism ; Culture Media ; chemistry ; Microbiological Techniques ; Nitrogen ; pharmacology ; Phanerochaete ; drug effects ; growth & development ; metabolism ; Temperature ; Time Factors

Adolescent ; Adult ; Air Pollutants, Occupational ; blood ; metabolism ; urine ; Humans ; Male ; Manganese ; blood ; metabolism ; urine ; Middle Aged ; Saliva ; chemistry ; Welding ; Young Adult

With the increasing occurrence of haze during the summer, the physicochemical characteristics and toxicity differences in PM_2.5 in different seasons are of great concern. Hangzhou is located in an area that has a subtropical monsoon climate where the humidity is very high during both the summer and winter. However, there are limited studies on the seasonal differences in PM_2.5 in these weather conditions. In this test, PM_2.5 samples were collected in the winter and summer, the morphology and chemical composition of PM_2.5 were analyzed, the toxicity of PM_2.5 to human bronchial cells BEAS-2B was compared, and the correlation between PM_2.5 toxicity and the chemical composition was discussed. The results showed that during both the winter and summer, the main compounds in the PM_2.5 samples were water-soluble ions, particularly SO₄^2-, NO₃^-, and NH₄⁺, followed by organic components, while heavy metals were present at lower levels. The higher the mass concentration of PM_2.5, the greater its impact on cell viability and ROS levels. However, when the mass concentration of PM_2.5 was similar, the water extraction from the summer samples showed a greater impact on BEAS-2B than that from the winter samples. The cytotoxicity of PM_2.5 was closely associated with heavy metals and organic pollutants but less related to water-soluble ions.
Air Pollutants/toxicity* ; Bronchi/metabolism* ; Carbon/chemistry* ; Environmental Monitoring ; Humans ; Ions ; Metals, Heavy ; Organic Chemicals ; Particle Size ; Particulate Matter/toxicity* ; Seasons ; Temperature ; Water

OBJECTIVEAir-borne particulates from different sources could have different physicochemical properties and inflammatory potentials. This study aims to characterize the chemical compositions and the toxicity of ambient particulate matter (PM) associated with traffic emissions.

METHODSThe concentrations of trace elements, organic carbon (OC), elemental carbon (EC) and polycyclic aromatic hydrocarbons (PAHs) in PM2.5 and PM10 were measured in samples collected at sites in Beijing, China. Their toxic effects on the pulmonary system of rats were investigated. Biochemical parameters (LDH, T-AOC, TP) and inflammatory cytokine(IL-6, IL-1, TNF-a) levels were measured in the lungs of rats exposed to traffic-related PM. Oxidative damage was observed. PM samples were taken from a near road site and an off road site in summer time in 2006.

RESULTSThe concentrations of the USEPA priority pollutant PAHs in both PM10 and PM2.5 were higher (299.658 and 348.412) at the near road site than those (237.728 and 268.472) at the off road site. The similar trend was observed for the concentrations of trace elements in PM. Compared to coarse particles (PM10), fine particles (PM2.5) have a greater adsorption capacity to enrich toxic elements than inhalable particles. Decrease in antioxidant capacity and an increase in the amount of lipid peroxidation products in rat lung tissues was observed.

CONCLUSIONThe findings of the present study suggest that the differing inflammatory responses of PM collected from the two road sites might have been mediated by the differing physicochemical characteristics.

Air Pollutants ; chemistry ; toxicity ; Animals ; Bronchoalveolar Lavage Fluid ; chemistry ; China ; Cities ; Cytokines ; genetics ; metabolism ; Gene Expression Regulation ; physiology ; Lung ; drug effects ; metabolism ; Male ; Particle Size ; Particulate Matter ; toxicity ; Rats ; Rats, Wistar ; Vehicle Emissions ; toxicity

Epidemiologic studies have suggested the association between environmental exposure to volatile organic compounds (VOCs) and polycyclic aromatic hydrocarbons (PAHs) and the increased risk of incurring asthma. Yet there is little data regarding the relationship between personal exposure to air pollution and the incidence of asthma in children. This study was designed to evaluate the effect of exposure to air pollution on children with asthma by using exposure biomarkers. We assessed the exposure level to VOCs by measuring urinary concentrations of hippuric acid and muconic acid, and PAHs by 1-OH pyrene and 2-naphthol in 30 children with asthma and 30 children without asthma (control). The mean level of hippuric acid was 0.158+/-0.169micromol/mol creatinine in the asthma group and 0.148+/-0.249micromol/mol creatinine in the control group, with no statistical significance noted (p=0.30). The mean concentration of muconic acid was higher in the asthma group than in the control group (7.630+/-8.915micromol/mol creatinine vs. 3.390+/-4.526micromol/mol creatinine p=0.01). The mean level of urinary 1-OHP was higher in the asthma group (0.430+/-0.343micromol/mol creatinine) than the control group (0.239+/-0.175micromol/mol creatinine), which was statistically significant (p=0.03). There was no difference in the mean concentration of 2-NAP between the two groups (9.864+/-10.037micromol/mol in the asthma group vs. 9.157+/-9.640micromol/mol in the control group, p=0.96). In conclusion, this study suggests that VOCs and PAHs have some role in asthma.
Air Pollutants/*pharmacology ; Asthma/*physiopathology/urine ; Case-Control Studies ; Child, Preschool ; Creatinine/urine ; Female ; Hippurates/urine ; Humans ; Male ; Naphthols/urine ; Organic Chemicals/chemistry/*pharmacology ; Polycyclic Hydrocarbons, Aromatic/*pharmacology ; Pyrenes/metabolism ; Sorbic Acid/*analogs & derivatives/metabolism ; Volatilization

OBJECTIVETo explore the source of the fine particulate matter (PM(2.5)) in the sarcoidosis granulomatous cell and the relationship between the sarcoidosis and the PM(2.5) in the atmosphere.

METHODSParaffin-embedded tissues of 50 cases of human sarcoidosis biopsy samples, 10 cases of non-sarcoidosis autopsy lung samples, 18 cases of lung tissues (with granulomatous lesions) of rats exposed to PM(2.5) by bronchial infusion, and the free PM(2.5) sample in the atmosphere were collected. The characteristics of tissues above mentioned were observed under the light microscopy, which stained by HE staining and Warthin-Starry silver staining. The characteristics of the PM(2.5) in the four groups were analyzed using confocal Raman microscopy. The component of the PM(2.5) in the sarcoidosis granuloma was analyzed using transmission electron microscope-energy dispersive X-ray detector (TEM-EDX), and the component of the PM(2.5) in the atmosphere was analyzed with X-ray fluorescence separately.

RESULTSThe PM(2.5) in the four groups have the similar Raman spectrum, they share the feature of carbonaceous composition, the element component of PM(2.5) in the human sarcoidosis was the same as PM(2.5) in the atmosphere.

CONCLUSIONThe study provided the further evidence that the PM(2.5) in the sarcoidosis lesion was from PM(2.5) in the atmosphere, and it should be not excepted that sarcoidosis may be a sensitive individual reaction to the PM(2.5) inhaled from the atmosphere.

Adolescent ; Adult ; Aged ; Air Pollutants ; analysis ; Aluminum ; analysis ; Animals ; Carbon ; analysis ; Child ; Female ; Granuloma ; metabolism ; pathology ; Granuloma, Respiratory Tract ; metabolism ; pathology ; Humans ; Lung ; chemistry ; Male ; Middle Aged ; Particle Size ; Particulate Matter ; analysis ; chemistry ; Rats ; Sarcoidosis ; metabolism ; pathology ; Sarcoidosis, Pulmonary ; metabolism ; pathology ; Silicon ; analysis ; Skin Diseases ; metabolism ; pathology ; Spectrum Analysis, Raman ; Young Adult

Accurate estimation of the exposure-response relationship between ambient urban particulate matters (PM) and public health is important for regulatory perspective of ambient urban particulate matters (PM). Ambient PM contains various transition metals and organic compounds. PM10 (aerodynamic diameter less than 10 microgram) is known to induce diverse diseases such as chronic cough, bronchitis, chest illness, etc. However, recent evaluation of PM2.5 (aerodynamic diameter less than 2.5 microgram) against health outcomes has suggested that the fine particles may be more closely associated with adverse respiratory health effects than particles of larger size. This study was performed to evaluate PM2.5-induced oxidative stress in rat lung epithelial cell in order to provide basic data for the risk assessment of PM2.5. PM2.5 showed higher cytotoxicity than PM10. Also, PM 2.5 induced more malondialdehyde (MDA) formation than PM10. In Hoechst 33258 dye staining and DNA fragmentation assay, apopotic changes were clearly detected in PM2.5 treated cells in compared to PM10. Expression of catalase mRNA was increased by PM2.5 rather than PM10. PM2.5 induced higher Mth1 mRNA than PM10. In pBR322 DNA treated with PM2.5, production of single strand breakage of DNA was higher than that of PM10. In Western blot analysis, PM2.5 induced more Nrf-2 protein, associated with diverse transcriptional and anti-oxidative stress enzymes, compared to PM10. Our data suggest that PM2.5 rather than PM10 may be responsible for PM-induced toxicity. Additional efforts are needed to establish the environmental standard of PM2.5.
Air Pollutants/chemistry/*toxicity ; Animals ; Apoptosis/physiology ; Benzimidazoles/metabolism ; Blotting, Western ; Cell Line ; Cell Survival/physiology ; DNA Fragmentation/physiology ; DNA Repair Enzymes/genetics/metabolism ; DNA-Binding Proteins/metabolism ; Epithelial Cells/drug effects/enzymology/pathology ; Formazans/metabolism ; GA-Binding Protein Transcription Factor ; Lipid Peroxides/metabolism ; Lung Diseases/*chemically induced/enzymology/pathology ; Oxidative Stress/*physiology ; RNA, Messenger/chemistry/genetics ; Rats ; Reverse Transcriptase Polymerase Chain Reaction ; Tetrazolium Salts/metabolism ; Transcription Factors/metabolism

OBJECTIVEThe effect of the silica nanoparticles (SNs) on lungs injury in rats was investigated to evaluate the toxicity and possible mechanisms for SNs.

METHODSMale Wistar rats were instilled intratracheally with 1 mL of saline containing 6.25, 12.5, and 25.0 mg of SNs or 25.0 mg of microscale SiO2 particles suspensions for 30 d, were then sacrificed. Histopathological and ultrastructural change in lungs, and chemical components in the urine excretions were investigated by light microscope, TEM and EDS. MDA, NO and hydroxyproline (Hyp) in lung homogenates were quantified by spectrophotometry. Contents of TNF-α, TGF-β1, IL-1β, and MMP-2 in lung tissue were determined by immunohistochemistry staining.

RESULTSThere is massive excretion of Si substance in urine. The SNs lead pulmonary lesions of rise in lung/body coefficients, lung inflammation, damaged alveoli, granuloma nodules formation, and collagen metabolized perturbation, and lung tissue damage is milder than those of microscale SiO2 particles. The SNs also cause increase lipid peroxidation and high expression of cytokines.

CONCLUSIONThe SNs result into pulmonary fibrosis by means of increase lipid peroxidation and high expression of cytokines. Milder effect of the SNs on pulmonary fibrosis comparing to microscale SiO2 particles is contributed to its elimination from urine due to their ultrafine particle size.

Air Pollutants ; toxicity ; Animals ; Dose-Response Relationship, Drug ; Lung ; drug effects ; pathology ; ultrastructure ; Male ; Microscopy, Electron, Transmission ; Nanoparticles ; toxicity ; Pulmonary Fibrosis ; chemically induced ; metabolism ; pathology ; Random Allocation ; Rats ; Rats, Wistar ; Silicon Dioxide ; toxicity ; Specific Pathogen-Free Organisms ; Spectrometry, X-Ray Emission ; Urine ; chemistry