Prostaglandin E2 and phagocytosis of inhaled particulate matter by airway macrophages in cystic fibrosis.

BACKGROUND: Exposure to particulate matter (PM) air pollution is associated with adverse health outcomes in children with cystic fibrosis (CF). Airway macrophages (AM) phagocytose and retain inhaled PM in vivo, and the area of carbon in AM reflects both inhaled PM dose and phagocytic function. Since airway prostaglandin-E2 (PGE2) is increased in CF, and PGE2 suppresses AM phagocytosis, we sought evidence for PGE2-mediated suppression of AM phagocytosis of inhaled carbonaceous PM in CF. METHODS: After informed consent, urine was obtained from 20 controls and 24 CF children. In the subgroup of older children, at least one induced sputum was done in 20 controls and 19 CF children. Urinary tetranor PGEM, the major metabolite of PGE2, and sputum PGE2 were measured by mass spectrometry. The area of carbon in AM was determined by image analysis. Exposure to PM was assessed by modelling and personal monitoring. The effect of either PGE2 or CF sputum supernatant on phagocytosis of diesel exhaust particle (DEP) by AM was assessed in vitro. Data were analysed by t-test. RESULTS: Both urinary tetranor PGEM (P<0.05), and sputum PGE2 (P<0.05) were increased in CF . Despite no difference in PM exposure between groups, the area of phagocytosed carbon by AM was decreased in children with CF (P<0.01). PGE2 suppressed phagocytosis of DEP by AM from both controls and CF (P<0.0001). CF sputum supernatant suppressed phagocytosis of DEP by AM (P<0.0001) in a PGE2-dependent manner. CONCLUSION: Increased PGE2 in the CF airway suppresses phagocytosis of inhaled PM by AM.

Reductions in urinary metabolites of exposure to household air pollution in pregnant, rural Guatemalan women provided liquefied petroleum gas stoves.

BACKGROUND: Household air pollution from solid fuels is a leading risk factor for morbidity and mortality worldwide. Pregnant women's exposure to polycyclic aromatic hydrocarbons (PAHs) and volatile organic compounds (VOCs), two components of solid-fuel smoke, is associated with adverse birth outcomes. Even with improved solid-fuel stoves, exposure to PAHs and VOCs remains high. Therefore, cleaner cooking fuels need to be prioritized. OBJECTIVE: We aimed to quantify exposure reduction to PAHs and VOCs among pregnant women in rural Guatemala with a liquefied petroleum gas (LPG) stove intervention. MATERIALS AND METHODS: Urine from pregnant women (N = 50) was collected twice: at <20 weeks gestation, when women cooked exclusively with wood, and 6-8 weeks after receiving an LPG stove. Metabolites of four PAHs and eight VOCs were analyzed. Concurrent with urine collection, personal 48-h PM2.5 exposure was measured. RESULTS: Women cooking exclusively with wood were exposed to high levels of particulate matter (PM2.5), which was reduced by 57% with the LPG stove. Urinary concentrations of total PAH metabolites (-37%), PMA (benzene metabolite; -49%), and CNEMA (acrylonitrile metabolite; -51%) were reduced. However, recent use of a wood-fired sauna bath led to large increases in excretion of urinary toxicant metabolites (+66-135%). CONCLUSIONS: This is the first study to report PAH and VOC reductions from an LPG stove intervention introduced during pregnancy. However, other sources of air pollution minimized the gains seen from using an LPG stove. Thus, all sources of air pollution must be addressed in concert to reduce exposures to levels that protect health.

The modification of indoor PM2.5 exposure to chronic obstructive pulmonary disease in Chinese elderly people: A meet-in-metabolite analysis.

BACKGROUND: Exposure to airborne fine particulate matter (PM2.5) has been associated with a variety of adverse health outcomes including chronic obstructive pulmonary disease (COPD). However, the linkages between PM2.5 exposure, PM2.5-related biomarkers, COPD-related biomarkers and COPD remain poorly elucidated. OBJECTIVES: To investigate the linkages between PM2.5 exposure and COPD outcome by using the meet-in-middle strategy based on urinary metabolic biomarkers. METHODS: A cross-sectional study was designed to illustrate the mentioned quadripartite linkages. Indoor PM2.5 and its element components were assessed in 41 Chinese elderly participants including COPD patients and their healthy spouses. Metabolic biomarkers involved in PM2.5 exposure and COPD were identified by using urinary metabolomics. The associations between PM2.5- and COPD-related biomarkers were investigated by statistics and metabolic pathway analysis. RESULTS: Seven metabolites were screened and identified with significant correlations to PM2.5 exposure, which were majorly involved in purine and amino acid metabolism as well as glycolysis. Ten COPD-related metabolic biomarkers were identified, which suggested that amino acid metabolism, lipid and fatty acid metabolism, and glucose metabolism were disturbed in the patients. Also, PM2.5 and its many elemental components were significantly associated with COPD-related biomarkers. We observed that the two kinds of biomarkers (PM2.5- and COPD-related) integrated in a locally connected network and the alterations of these metabolic biomarkers can biologically link PM2.5 exposure to COPD outcome. CONCLUSIONS: Our study indicated the modification of PM2.5 to COPD via both modes of action of lowering participants' antioxidation capacity and decreasing their lung energy generation; this information would be valuable for the prevention strategy of COPD.

Cancer risk from polycyclic aromatic compounds in fine particulate matter generated from household coal combustion in Xuanwei, China.

Polycyclic aromatic hydrocarbons (PAHs) and their polar derivatives (oxygenated PAHs: OPAHs and azaarenes: AZAs) were characterized in fine particulates (PM2.5) emitted from indoor coal combustion. Samples were collected in Xuanwei (Yunnan Province), a region in China with a high rate of lung cancer. A sample from the community with the highest mortality contained the highest total concentration of PAHs, OPAHs and AZAs and posed the highest excess cancer risk from a lifetime of inhaling fine particulates. Positive correlations between total carbonyl-OPAHs, total AZAs and total PAHs implied that the emissions were dependent on similar factors, regardless of sample location and type. The calculated cancer risk ranged from 5.23-10.7 × 10-3, which is higher than the national average. The risk in each sample was ∼1-2 orders of magnitude higher than that deemed high risk, suggesting that the safety of these households is in jeopardy. The lack of potency equivalency factors for the PAH derivatives could possibly have underestimated the overall cancer risk.

Comparative study of oxidative stress biomarkers in urine of cooks exposed to three types of cooking-related particles.

OBJECTIVES: To evaluate how exposure to deep-frying oils, repeated frying oil (RFO) and restaurant waste oil (RWO) affects emission of polycyclic aromatic hydrocarbons (PAHs) and oxidative stress in male restaurant workers. METHODS: The study participants included 236 male restaurant workers in 12 restaurants in Shenzhen. Airborne particulate PAHs were measured over 12h on each of two consecutive work days. Urinary 1-hydroxypyrene (1-OHP) measurements were used to indicate cooking oil fumes (COF) exposure, and urinary malondialdehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were adopted as oxidative stress markers. RESULTS: The production and emission rates of ultrafine particles (UFPs) and PM2.5 were higher in the exposed groups than in the control group. The concentrations of summed PAHs were in the order of RFO-frying group>RWO-frying group>deep-frying group>unexposed control group. Urinary 1-OHP was found to be a significant predictor of elevated urinary MDA and 8-OHdG concentrations (all, P<0.05). UFPs were a significant predictor of elevated urinary 8-OHdG for restaurant workers (P<0.05). The RFO- and RWO-frying groups had higher mean urinary concentrations of 1-OHP, MDA and 8-OHdG than the control group (P<0.05). RFO exposure was found to be a significant risk factor for elevated urinary 8-OHdG and RWO exposure was found to be a significant risk factor for elevated urinary MDA (both, P<0.001). CONCLUSIONS: Concentrations of urinary 1-OHP, MDA and 8-OHdG reflect occupational exposure to PAHs from COFs and oxidative stress in restaurants workers. Exposure to RFO may cause increased oxidative DNA damage, and exposure to RWO might cause increased lipid peroxidation.

Urinary polycyclic aromatic hydrocarbon metabolites as biomarkers to woodsmoke exposure - results from a controlled exposure study.

Woodsmoke contains harmful components - such as fine particulate matter (PM2.5) and polycyclic aromatic hydrocarbons (PAHs) - and impacts more than half of the global population. We investigated urinary hydroxylated PAH metabolites (OH-PAHs) as woodsmoke exposure biomarkers in nine non-smoking volunteers experimentally exposed to a wood fire. Individual urine samples were collected from 24-h before to 48-h after the exposure and personal PM2.5 samples were collected during the 2-h woodsmoke exposure. Concentrations of nine OH-PAHs increased by 1.8-7.2 times within 2.3-19.3 h, and returned to baseline approximately 24 h after the exposure. 2-Naphthol (2-NAP) had the largest post-exposure increase and exhibited a clear excretion pattern in all participants. The level of urinary OH-PAHs, except 1-hydroxypyrene (1-PYR), correlated with those of PM2.5, levoglucosan and PAHs in personal PM2.5 samples. This finding suggests that several urinary OH-PAHs, especially 2-NAP, are potential exposure biomarkers to woodsmoke; by contrast, 1-PYR may not be a suitable biomarker. Compared with levoglucosan and methoxyphenols - two other urinary woodsmoke biomarkers that were measured in the same study and reported previously - OH-PAHs might be better biomarkers based on sensitivity, robustness and stability, particularly under suboptimal sampling and storage conditions, like in epidemiological studies carried out in less developed areas.

Assessment of the levels of urinary 1-hydroxypyrene and air polycyclic aromatic hydrocarbon in PM2.5 for adult exposure to the petrochemical complex emissions.

The relationship between external exposure and internal doses of polycyclic aromatic hydrocarbons (PAHs) has not been established for people living in industrial areas. This study was carried out to estimate the relationship between particle-phase PAH exposure and urinary 1-hydroxypyrene (1-OHP) levels among the adults living near a large petrochemical complex in Mailiao, Taiwan. We measured urinary 1-OHP in 781 residents above 35 years old and PM2.5 PAHs within a 20-km radius downwind from the petrochemical complex. Urinary 1-OHP was analyzed by high performance liquid chromatography, while 16 ambient particle-phase PAHs were measured by gas chromatography mass spectrometry. External exposures to individual PAHs at each study subject's address were estimated by kriging interpolation from air sampling results and regressed against the subjects' urinary 1-OHP levels, adjusting for confounding factors. The study population's urinary 1-OHP levels ranged from 0.001 to 3.005 µmol/mol-creatinine with significantly higher levels for females, grilled food consumers, and residents living close to roads. All 16 particle-phase PAHs were present in the study area with total PAH concentrations ranging from 0.111 to 1.982 ng/m(3). The spatial distribution of 4- and 5-ring PAHs identified high-concentration hotspots close to the complex in Mailiao. The multiple regression models showed that the adults' urinary 1-OHP levels were significantly correlated with 5 out of the 16 PAHs, including benzo[a]anthracene, benzo[k]fluoranthene, fluoranthene, pyrene, and dibenzo[a,h]anthracene; a 0.01 ng/m(3) increase in the concentration of these 5 PAHs at the study subjects' addresses was associated with a 20% elevation in urinary 1-OHP levels (µg/g-creatinine). Emissions from a petrochemical complex can elevate particle-phase PAH concentrations in surrounding areas and increase the urinary 1-OHP levels of adults living nearby.

Determination of parent and hydroxy PAHs in personal PM2.5 and urine samples collected during Native American fish smoking activities.

A method was developed for the measurement of 19 parent PAHs (PAHs) and 34 hydroxylated PAHs (OH-PAHs) in urine and personal air samples of particulate matter less than 2.5 µm in diameter (PM2.5) using GC-MS and validated using NIST SRM 3672 (Organic Contaminants in Smoker's Urine) and SRM 3673 (Organic Contaminants in Nonsmoker's Urine). The method was used to measure PAHs and OH-PAHs in urine and personal PM2.5 samples collected from the operators of two different fish smoking facilities (tipi and smoke shed) burning two different wood types (alder and apple) on the Confederated Tribes of Umatilla Indian Reservation (CTUIR) while they smoked salmon. Urine samples were spiked with ß-glucuronidase/arylsulfatase to hydrolyze the conjugates of OH-PAHs and the PAHs and OH-PAHs were extracted using Plexa and C18 solid phases, in series. The 34 OH-PAHs were derivatized using MTBSTFA, and the mixture was measured by GC-MS. The personal PM2.5 samples were extracted using pressurized liquid extraction, derivatized with MTBSTFA and analyzed by GC-MS for PAHs and OH-PAHs. Fourteen isotopically labeled surrogates were added to accurately quantify PAHs and OH-PAHs in the urine and PM2.5 samples and three isotopically labeled internal standards were used to calculate the recovery of the surrogates. Estimated detection limits in urine ranged from 6.0 to 181 pg/ml for OH-PAHs and from 3.0 to 90 pg/ml for PAHs, and, in PM2.5, they ranged from 5.2 to 155 pg/m(3) for OH-PAHs and from 2.5 to 77 pg/m(3) for PAHs. The results showed an increase in OH-PAH concentrations in urine after 6h of fish smoking and an increase in PAH concentrations in air within each smoking facility. In general, the PAH exposure in the smoke shed was higher than in the tipi and the PAH exposure from burning apple wood was higher than burning alder.

Clinical application of UF-1000i in combination with AX-4280 for the screening test ability of urinary formed elements.

AIMS: To evaluate the screening test ability of UF-1000i combination with AX-4280 for major pathological urinary formed elements and to establish screening rules suitable for our laboratory. METHODS: A total of 2220 cases of urine samples were collected from out-patients and inpatients. The sample tests were finished within 4 h after collection. The results were verified and corroborated with microscopic tests. RESULTS: In 'both-negative' group, the negative predictive values for red blood cell, white blood cell and cast were 99.12%, 99.56% and 100%, respectively, and the false negative rates were 0.87%, 0.44% and 0%, respectively. In 'both-positive' group, the positive predictive values for red blood cell, white blood cell and cast were 69.18%, 74.41% and 33.33%, respectively, and the false positive rates were 30.82%, 25.59% and 66.67%, respectively. In 'U positive/A negative' group, the positive predictive values for red blood cell, white blood cell and cast were 32.47%, 23.67% and 8.57%, respectively, and the false positive rates were 67.53%, 76.36% and 91.43%, respectively. In 'U negative/A positive' group, the positive predictive values for red blood cell, white blood cell and cast were 8.18%, 19.50% and 4.67%, respectively, and the false positive rates were 91.82%, 50.50% and 95.24%, respectively. CONCLUSIONS: When the results of the red blood cell, white blood cell and cast tested by UF-1000i were all negative, and the results of the red blood cell, white blood cell and protein tested by AX-4280 were negative, an automatic report stating 'normal microscopic appearance' was generated, and then the microscopic test rate was reduced by 37.6%. However, if any automated parameter measurement was out of the reference range, corroboration by manual microscopy was advisable.

Activation of protein kinase B (PKB/Akt) and risk of lung cancer among rural women in India who cook with biomass fuel.

The impact of indoor air pollution (IAP) from biomass fuel burning on the risk of carcinogenesis in the airways has been investigated in 187 pre-menopausal women (median age 34years) from eastern India who cooked exclusively with biomass and 155 age-matched control women from same locality who cooked with cleaner fuel liquefied petroleum gas. Compared with control, Papanicolau-stained sputum samples showed 3-times higher prevalence of metaplasia and 7-times higher prevalence of dysplasia in airway epithelial cell (AEC) of biomass users. Immunocytochemistry showed up-regulation of phosphorylated Akt (p-Akt(ser473) and p-Akt(thr308)) proteins in AEC of biomass users, especially in metaplastic and dysplastic cells. Compared with LPG users, biomass-using women showed marked rise in reactive oxygen species (ROS) generation and depletion of antioxidant enzyme, superoxide dismutase (SOD) indicating oxidative stress. There were 2-5 times more particulate pollutants (PM(10) and PM(2.5)), 72% more nitrogen dioxide and 4-times more particulate-laden benzo(a)pyrene, but no change in sulfur dioxide in indoor air of biomass-using households, and high performance liquid chromatography estimated 6-fold rise in the concentration of benzene metabolite trans,trans-muconic acid (t,t-MA) in urine of biomass users. Metaplasia and dysplasia, p-Akt expression and ROS generation were positively associated with PM and t,t-MA levels. It appears that cumulative exposure to biomass smoke increases the risk of lung carcinogenesis via oxidative stress-mediated activation of Akt signal transduction pathway.

Evaluation of exposure reduction to indoor air pollution in stove intervention projects in Peru by urinary biomonitoring of polycyclic aromatic hydrocarbon metabolites.

Burning biomass fuels such as wood on indoor open-pit stoves is common in developing regions. In such settings, exposure to harmful combustion products such as fine particulate matter (PM(2.5)), carbon monoxide (CO) and polycyclic aromatic hydrocarbons (PAHs) is of concern. We aimed to investigate if the replacement of open pit stoves by improved stoves equipped with a chimney would significantly reduce exposure to PAHs, PM(2.5) and CO. Two stove projects were evaluated in Peru. Program A was part of the Juntos National Program in which households built their own stoves using materials provided. In Program B, Barrick Gold Corporation hired a company to produce and install the stoves locally. A total of 30 and 27 homes participated in Program A and B, respectively. We collected personal and kitchen air samples, as well as morning urine samples from women tasked with cooking in the households before and after the installation of the improved stoves. Median levels of PM(2.5) and CO were significantly reduced in kitchen and personal air samples by 47-74% after the installation of the new stoves, while the median reduction of 10 urinary hydroxylate PAH metabolites (OH-PAHs) was 19%-52%. The observed OH-PAH concentration in this study was comparable or higher than the 95th percentile of the general U.S. population, even after the stove intervention, indicating a high overall exposure in this population.

Environmental tobacco smoke exposure among casino dealers.

OBJECTIVE: This study quantified casino dealers' occupational exposure to environmental tobacco smoke (ETS). METHODS: We measured casino dealers' exposure to ETS components by analyzing full-shift air and preshift and postshift urine samples. RESULTS: Casino dealers were exposed to nicotine, 4-vinyl pyridine, benzene, toluene, naphthalene, formaldehyde, acetaldehyde, solanesol, and respirable suspended particulates. Levels of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) in urine increased significantly during an 8-hour work shift both with and without adjustment for creatinine clearance. Creatinine-unadjusted cotinine significantly increased during the 8-hour shift, but creatinine-adjusted cotinine did not increase significantly. CONCLUSIONS: Casino dealers at the three casinos were exposed to airborne ETS components and absorbed an ETS-specific component into their bodies, as demonstrated by detectable levels of urinary NNAL. The casinos should ban smoking on their premises and offer employee smoking cessation programs.

Urine particles analysis: performance evaluation of Sysmex UF-1000i and comparison among urine flow cytometer, dipstick, and visual microscopic examination.

INTRODUCTION: Our objective was to evaluate a newly invented urine flow cytometer, and select an optimal strategy for urinalysis in clinical practice. METHODS: The performance of UF-1000i was evaluated in both control material and patient samples. A total of 1631 specimens were collected and analysed by visual microscopy examination (VME), UF-1000i flow cytometer (Sysmex Medical Electronics Co, Kobe, Japan) and an automated dipstick reflectometer Clinitek Atlas (Bayer Corp, Elkhart, USA). RESULTS: UF-1000i showed good imprecision performance for the main parameters in urine particles with CV values less than 20%. The results from UF-1000i correlated well with VME for erythrocytes (r = 0.96), leukocytes (r = 0.98), and epithelial cell (r = 0.84). The area under the receiver operating curve (AUC) was 0.879, 0.903, 0.783, and 0.817 respectively for erythrocytes, leukocytes, bacteria and CAST in UF-1000i. While in Clinitek Atlas, the AUC was 0.848, 0.803, 0.761, and 0.754 respectively. Sensitivity of combination of the two methods for screening remained at 98% as compared to VME alone, while reducing the visual review rate down to 40%. CONCLUSION: UF-1000i is capable of reproducible measurement of urine particles in the clinically relevant range and shows its advantage over Atlas. Combination of the two methods is an optimal strategy for urine sample screening.

Personal exposure to particulate PAHs and anthraquinone and oxidative DNA damages in humans.

Recent studies suggest that DNA oxidative damage be related to the chemical constituents of ambient particles. The purpose of this study was to examine whether particulate polycyclic aromatic hydrocarbons (PAHs) and quinone-structure chemicals increase body burden of oxidative stress in human exposed to heavy traffic volume. We recruited two nonsmoking security guards who worked at a university campus gate near a heavily trafficked road. Each subject wore a personal air sampler for 24h per day to estimate exposures to 24 PAHs and anthraquinone (AnQ) in PM(2.5). Daily pre- and post-work shift spot urines were collected for 29d from each subject. Urine samples were analyzed for 8-hydroxy-2'-deoxyguanosine (8-OHdG). Additionally, using 19 organic tracers other than 24 PAHs and AnQ, a receptor source apportionment model of chemical mass balance was applied to determine the contributions of sources on the PM: gasoline vehicle, diesel vehicle, coal burning, vegetable debris, cooking, natural gas and biomass burning. The relationship among urinary 8-OHdG, individual PAH, and AnQ was demonstrated as follows: the average urinary concentration of 8-OHdG was increased more than three times after 8-h work-shift than those before the work shift. All the 24 PAH and AnQ levels were positively and significantly associated with the post-work urinary 8-OHdG. The results from source apportionment suggest vehicular emission to be the dominant source of personal exposure to PM(2.5). Our finding indicates that personal air exposures to 24 individual PAHs and AnQ originating from traffic emissions are important in increasing oxidative burdens in human body.

Airborne particulate metals in the New York City subway: a pilot study to assess the potential for health impacts.

A prior study in New York City observed that airborne concentrations of three metals found in steel - iron, manganese, and chromium - are more than 100 times higher in the subway system than in aboveground air. To investigate the potential for health effects of exposure at these levels, we conducted a pilot study of subway workers comparing personal exposures to steel dust with biomarkers of metal exposure, oxidative stress, and DNA damage in blood and urine samples. Workers wore a personal air sampler operating at 4L/m for one to three work shifts with blood and urine samples collected at the end of the final shift. We found that PM(2.5) exposures varied among subway workers on the basis of job title and job activity. The subway workers' mean time-weighted PM(2.5) exposure was 52 microg/m3, with a median of 27 microg/m3, and a range of 6-469 microg/m3. The observed concentrations of PM(2.5), iron, manganese, and chromium fell well below occupational standards. Biomarker concentrations among the 39 subway workers were compared with a group of 11 bus drivers, and a group of 25 suburban office workers. Concentrations of DNA-protein crosslinks and chromium in plasma were significantly higher in subway workers than in bus drivers, but no significant difference was observed for these biomarkers between subway workers and office workers. Urinary isoprostane concentrations were significantly correlated with the number of years working in the subway system, and were detected at higher, though not significantly higher, concentrations in subway workers than in bus drivers or office workers. At the group level, there was no consistent pattern of biomarker concentrations among subway workers significantly exceeding those of the bus drivers and office workers. At the individual level, steel dust exposure was not correlated with any of the biomarkers measured.

Exposure assessment of PM2.5 and urinary 8-OHdG for diesel exhaust emission inspector.

Animal studies have shown exposure to diesel exhaust particles (DEPs) to induce production of reactive oxygen species (ROSs) and increase levels of 8-hydroxydeoxyquanosine (8-OHdG). Controversial results have been obtained regarding the effects of workplace exposure on urinary 8-OHdG level. This study assessed concentrations of environmental PM(2.5) in DEP (DEP(2.5)), personal DEP(2.5) and urinary 8-OHdG of diesel engine exhaust emission inspector (inspector) at a diesel vehicle emission inspection station (inspection station). The analysis specifically focuses on the factors that influence inspector urinary 8-OHdG. Repeated-measures study design was used to sample for five consecutive days. A total of 25 environmental PM(2.5) measurements were analyzed at 5 different locations by using a dichotomous sampler, and a total of 55 personal PM(2.5) measurements were analyzed from inspectors by using PM(2.5) personal sampler. During the sampling period, a total of 110 pre- and post-work urine samples from inspectors, and 32 samples from the control group were collected. Following age and sex matching between the inspectors and the control group, levels of urinary 8-OHdG were analyzed. Environmental and personal concentrations of DEP(2.5) were 107.25+/-39.76 (mean+/-SD) and 155.96+/-75.70 microg/m(3), respectively. Also, the concentration of urinary 8-OHdG differed significantly between inspector and control non-smokers, averaging 14.05+/-12.71 and 6.58+/-4.39 microg/g creatinine, respectively. Additionally, urinary 8-OHdG concentrations were associated with diesel exposure after controlling for smoking and cooking at home. Compared with the control group, the inspector displayed significantly increased levels of urinary 8-OHdG. Diesel exhaust is the single pollutant involved in the exposure of DEP(2.5) at the inspection station, as confirmed by the final results.

Effects of diesel vehicle emissions of polycyclic aromatic hydrocarbons on the surrounding environment and residents.

Ten stations alongside major thoroughfares were selected as exposure sites, while a small village located about 3 kilometers away from a main traffic route was selected as the control site. The concentrations of particulate matters with aerodynamic less than 2.5 microm (PM(2.5)) and elemental carbon (EC) at exposure sites were both higher than those at the control site. Daytime mean concentrations of total polycyclic aromatic hydrocarbons (t-PAHs), carcinogenic PAHs (car-PAHs), and Benzo(a)pyrene-equivalent dose (BaP(eq)) at exposure sites were all about twice as high as those at the control site. A significant relationship between t-PAHs and EC was found, suggesting that most of the t-PAHs at exposure sites were contributed by diesel exhaust. Furthermore, the diagnostic ratios also show that diesel emissions were the dominant sources of PAHs at exposure sites. A multiple linear regression was applied to urinary 1-hydroxyprene (1-OHP) using four variables (exposure status, sex, smoker status, and incense burning) as independent variables. The results showed that the concentrations of 1-OHP in exposure groups were significantly (p < 0.001) higher than those in the control group. The explainable percentage for exposure status was 91.1%, indicating that the exposure factor, in comparison with other factors, has a dominant contribution to the concentration of 1-OHP. After subtracting the background levels of 1-OHP, the levels of urinary 1-OHP for residents exposed to the exhaust of 100 vehicles were about 0.062 microg/g creatinine.

Seasonal and regional contributors of 1-hydroxypyrene among children near a steel mill.

Urinary 1-hydroxypyrene (1-OHP) is a biomarker of exposure to polycyclic aromatic hydrocarbons (PAH). Effect of residence on children's PAH exposure was reported among children living near a polluted area. Instead of a snapshot assessment, however, a temporal history of exposure characteristics needs to be assessed in the studies of chronic disease development such as cancer. The urinary 1-OHP measurements were repeated to determine regional effect of ambient air pollution on 1-OHP levels over extended periods. Two sites were chosen: (a) one site located near the steel mill ("nearby" site) and (b) the other site located at a longer distance from the mill ("remote" site). Spot urinary 1-OHP levels were measured from 72 children for 3 consecutive days per month, repeated over 9-month period. Compared with remote site, the nearby site had increased the urinary 1-OHP level by 62.3% [95% confidence interval (95% CI), 39.8-88.3%]. Other statistically significant factors that contributed to the level include sex [16.5% (95% CI, 1.2-34.1%) higher for girls than boys], consumption of charbroiled meat [16.5% (95% CI, 1.1-34.2%) higher], and an increase in PM(10) [10.1% (95% CI, 4.8-15.7%) higher for the interquartile range increment]. Controlling for covariates, the 1-OHP levels were increased in the summer and fall compared with winter. The magnitude of the effects of both seasons had diminished after adjusting for PM(10). This is the first report providing seasonal and regional contributors to environmental PAH exposure, assessed by urinary 1-OHP, with higher 1-OHP levels during summer when ambient pollution was also high.

Urinary 8-oxodeoxyguanosine levels in children exposed to air pollutants.

Oxidative stress is believed to be one of the mechanisms of effects of air pollution to human health. We investigated levels of 8-oxodeoxyguanosine (8-oxodG), a marker of oxidative damage to DNA, in urine samples of 894 children from two districts in the Czech Republic: Teplice and Prachatice. We assessed the association between 8-oxodG levels and exposure to particulate matter of different size:

Urinary 8-isoprostane and 8-OHdG concentrations in boilermakers with welding exposure.

OBJECTIVE: To investigate the association of exposure to fine particulate matter (PM2.5) with DNA damage and oxidative stress in boilermakers exposed to welding fumes. METHODS: Forty-one workers were monitored over 24 hours during which baseline, postshift, bedtime, and next morning measurements were collected. Twenty-two workers participated as controls. RESULTS: Linear regression was used to model pairwise change in u-8-isoprostane and u-8-OHdG: pre- to postshift, preshift to bedtime, postshift to bedtime, and postshift to next morning. In the models, pre- to postshift change in 8-OHdG was statistically significant, whereas postshift to bedtime change in 8-isoprostane showed an unexpected inverse relationship with PM2.5. CONCLUSIONS: Acute welding exposure is associated with a postshift blunting of systemic inflammation in chronically exposed boilermakers, as measured by 8-isoprostane. The level of oxidative DNA damage as measured by 8-OHdG is less clear.