Polycyclic Aromatic Hydrocarbons Exposure Levels Research Articles

Polycyclic aromatic hydrocarbons exposure decreased sperm mitochondrial DNA copy number: A cross-sectional study (MARHCS) in Chongqing, China

Polycyclic aromatic hydrocarbons (PAHs) are widespread environmental pollutants that have adverse effects on the male reproductive function. Many studies have confirmed that PAHs preferentially accumulate in mitochondria DNA relative to nuclear DNA and disrupt mitochondrial functions. However, it is rare whether exposure to PAHs is associated with mitochondrial damage and dysfunction in sperm. To evaluate the effects of PAHs on sperm mitochondria, we measured mitochondrial membrane potential (MMP), mitochondrial DNA copy number (mtDNAcn) and mtDNA integrity in 666 individuals from the Male Reproductive Health in Chongqing College Students (MARHCS) study. PAHs exposure was estimated by measuring eight urinary PAH metabolites (1-OHNap, 2-OHNap, 1-OHPhe, 2-OHPhe, 3-OHPhe, 4-OHPhe, 2-OHFlu and 1-OHPyr). The subjects were divided into low, median and high exposure groups using the tertile levels of urinary PAH metabolites. In univariate analyses, the results showed that increased levels of 2-OHPhe, 3-OHPhe, ∑Phe metabolites and 2-OHFlu were found to be associated with decreased sperm mtDNAcn. After adjusting for potential confounders, significantly negative associations of these metabolites remained (p = 0.039, 0.012, 0.01, 0.035, respectively). Each 1 μg/g creatinine increase in 2-OHPhe, 3-OHPhe, ∑Phe metabolites and 2-OHFlu was associated with a decrease in sperm mtDNAcn of 9.427%, 11.488%, 9.635% and 11.692%, respectively. There were no significant associations between urinary PAH metabolites and sperm MMP or mtDNA integrity. The results indicated that the low exposure levels of PAHs can cause abnormities in sperm mitochondria.

High-throughput microfluidic platform for culture of 3D kidney tissue models

Polycyclic aromatic hydrocarbons (PAHs) are a group of ubiquitous environmental pollutants. In vivo and in vitro studies have demonstrated that PAHs can alter endocrine function, yet evidence from human studies is limited.The objective of this study was to investigate whether environmental exposure to PAHs was associated with altered reproductive hormone levels, using repeated measures of urinary OH-PAHs as biomarkers.We measured 10 monohydroxylated PAHs (OH-PAHs) in repeated urine samples from 371 men in an infertility clinic in Wuhan, China. Multivariable linear regression models were used to estimate the associations between average urinary OH-PAH levels and serum reproductive hormones, and restricted cubic spline models were further used to examine the shapes of dose-response relationships.We observed dose-response associations of urinary 2-hydroxynaphthalene (2-OHNa) with decreased serum free testosterone (fT) and urinary 1-hydroxypyrene (1-OHP), 9-hydroxyphenanthrene (9-OHPh), and 9-hydroxyfluorene (9-OHFlu) with decreased serum estradiol (all P for trends <0.05). These associations were linear and significant when these four OH-PAHs were modeled as continuous variables in restricted cubic spline models. Furthermore, a U-shaped association was observed across urinary 4-OHPh levels, with lower levels of serum sex hormone-binding globulin (SHBG) at median concentrations compared with 5th and 95th percentile concentrations.Environmental levels of PAH exposure in our study are associated with altered reproductive hormones. However, further research is needed to confirm our findings.

Exposure and size distribution of nitrated and oxygenated polycyclic aromatic hydrocarbons among the population using different household fuels

Polycyclic aromatic hydrocarbons (PAHs) derivatives like nitrated and oxygenated PAHs are of growing concerns because of considerably higher toxicity and important roles during atmospheric chemical reactions. Residential solid fuel combustion is likely to be one large primary source of these pollutants in developing countries. In this study, inhalation exposure to nitrated and oxygenated PAH derivatives was evaluated among rural residents using carried samplers. The exposure levels of individual nitrated PAHs ranged from 4.04 (9-nitrated phenanthrene) to 89.8 (9-nitrated anthracene) pg/m3, and of oxy-PAHs were 0.570 (benzo[a]anthracene-7, 12-dione) to 7.99 (Benzanthrone) ng/m3, generally higher in wood user than that in anthracite user. A majority of derivatives in particle presented in PM2.5 (80% for nitrated naphthalene and over 90% for other targets) and even fine PM1.0. Mass fractions of PAH derivatives in fine and ultra-fine particles were significantly higher than the fractions of corresponding parent PAHs, indicating more adverse health outcomes induced by these derivatives. The inhalation exposure levels for residents adopting wood gasifier burners was significantly lower than the documented results for those burning wood in typical built-in brick stoves, and comparable to those using LPG and electricity, which provided vital information for clean stove development and intervention programs.

Essential Metals Zinc, Selenium, and Strontium Protect against Chromosome Damage Caused by Polycyclic Aromatic Hydrocarbons Exposure.

Essential metals play important roles in maintaining cellular homeostasis, but the effects of their interaction with the environmental pollutants are still not very well-known in human subjects. The aim of this study was to evaluate the roles of essential metals and their interactions with polycyclic aromatic hydrocarbons (PAHs) on chromosome damage, an early carcinogenic event. A total of 1245 male workers were included in this study and the levels of 11 urinary essential metals, 12 urinary PAH metabolites, plasma concentrations of benzo[a]pyrene-r-7,t-8,t-9,c-10-tetrahydotetrol-albumin (BPDE-Alb) adducts, and lymphocyte micronucleus (MN) frequencies were monitored. We found that zinc (Zn), selenium (Se), and strontium (Sr) have significant inverse dose-response relationships with MN frequencies (all P < 0.05). Furthermore, the protective roles of Zn, Se, and Sr were mainly shown among subjects with high levels of BPDE-Alb adducts. Significant effect modification of BPDE-Alb adducts on the associations of Zn, Se, and Sr with MN frequencies was observed (all Pinteraction < 0.05). Our study showed evidence that Zn, Se, and Sr play protective roles in reducing chromosome damage, and these effects can be modified by PAH exposure levels. These findings add potential evidence for the preventive effects of Zn, Se, and Sr against carcinogenesis in human subjects.

Specific long non-coding RNAs response to occupational PAHs exposure in coke oven workers.

To explore whether the alteration of lncRNA expression is correlated with polycyclic aromatic hydrocarbons (PAHs) exposure and DNA damage, we examined PAHs external and internal exposure, DNA damage and lncRNAs (HOTAIR, MALAT1, TUG1 and GAS5) expression in peripheral blood lymphocytes (PBLCs) of 150 male coke oven workers and 60 non-PAHs exposure workers. We found the expression of HOTAIR, MALAT1, and TUG1 were enhanced in PBLCs of coke oven workers and positively correlated with the levels of external PAHs exposure (adjusted Ptrend<0.001 for HOTAIR and MALAT1, adjusted Ptrend=0.006 for TUG1). However, only HOTAIR and MALAT1 were significantly associated with the level of internal PAHs exposure (urinary 1-hydroxypyrene) with adjusted β=0.298, P=0.024 for HOTAIR and β=0.090, P=0.034 for MALAT1. In addition, the degree of DNA damage was positively associated with MALAT1 and HOTAIR expression in PBLCs of all subjects (adjusted β=0.024, P=0.002 for HOTAIR and β=0.007, P=0.003 for MALAT1). Moreover, we revealed that the global histone 3 lysine 27 trimethylation (H3K27me3) modification was positively associated with the degree of genetic damage (β=0.061, P<0.001) and the increase of HOTAIR expression (β=0.385, P=0.018). Taken together, our findings suggest that altered HOTAIR and MALAT1 expression might be involved in response to PAHs-induced DNA damage.

Cancer risk of petrochemical workers exposed to airborne PAHs in industrial Lanzhou City, China.

This paper reports the connections between red blood cells abnormality risk of petrochemical workers and their exposure to airborne polycyclic aromatic hydrocarbons (PAHs). Urinary 1-hydroxypyrene (1-OHP), as the biomarker of PAHs exposure, was adopted to assess the exposure risk of the petrochemical workers to PAHs in Xigu, the west suburb of Lanzhou where petrochemical industries are located. Fifty-three workers, sub-grouped to 36 petrochemical workers and 17 office workers, participated in this investigation. Logistic regression model and spearman correlation analysis were performed to estimate the associations between PAHs exposure levels and red blood cells abnormality risk of petrochemical workers. Strong associations between some red cell indices (MCH, MCHC, RDW) and 1-OHP concentration were found. Results also show that the red blood cells abnormality risk increased with increasing PAHs exposure level. Compared with office workers, risk level of red blood cells abnormality in petrochemical workers was higher by 41.7 % (OR, 1.417; 95 % CI: 0.368-5.456) than that in office workers. This result was verified by the tissue-to-human blood partition coefficient for pyrene and 1-OHP. The quantitative assessments of the potential health risk through inhalation exposure to PAHs were conducted using the Incremental Lifetime Cancer Risk (ILCR) model. It was found the ILCR from inhalation exposure to PAHs for the petrochemical workers ranged from 10(-5) to 10(-4) with 95 % probability, indicating that petrochemical plant workers were under a high potential cancer risk level.

Abstract 831: In utero polycyclic aromatic hydrocarbons exposure and genome-wide DNA methylation modifications at birth in children who develop acute lymphoblastic leukemia

Abstract Introduction Previously, residential dust content of polycyclic aromatic hydrocarbons (PAHs) was associated with an increased risk of acute lymphoblastic childhood leukemia (ALL), and PAHs exposure levels have been associated with differentially methylated regions (DMRs) in candidate genes studies. Thus, we hypothesized that in utero exposure to residential PAHs may be associated with genome-wide DMRs in genes that may influence ALL development. Methods PAHs were measured in dust samples collected using a high-volume surface sampler or household vacuum cleaners from homes of California Childhood Leukemia Study participants who have lived in the same home since diagnosis. The different PAHs were summed according to their toxic equivalency. DNA was extracted from archived neonatal blood spots of participants, then treated with bisulfite and assayed on Illumina Infinium 450K genome-wide DNA methylation arrays. Following removal of cross-reacting probes, SNP-related and polymorphic CpGs, we analyzed the association of residential PAH levels with methylation intensity of 319,265 CpGs in two independent case-only datasets (model #1: set 1 cases n = 84, set 2 cases n = 51). We used a false discovery rate with random resampling to reduce the number of false-positive findings and cross-validated the results between sets. This first step of the analysis gave 11 significant and sign concordant CpGs. Then we assessed interactions between case/control status and PAHs levels with methylation intensities at those 11 CpGs in set 1 (model #2: total cases and controls n = 306). Models were adjusted for cell mixture, sex, gestational age, race and the first 2 principal components of the models’ residuals. Results In model #1, methylation levels at 11 CpGs were significantly associated with residential PAH levels and sign concordant in both sets with a corresponding q-value &amp;lt; 10−08. In model #2, the interaction terms between PAH and case/control status were significant (p&amp;lt;0.05) in 7 of these 11 CpGs, and the 3 most significant were: cg13484813 (p &amp;lt;0.001) in LGR5 (chr12q21.1) which is differentially expressed in pre-B cell vs. leukemia cells; cg23196133 (p &amp;lt;0.01) in ZBTB4 (chr17p13.1) which is a transcription factor linked to p53; and cg07617339 (p &amp;lt;0.01) in ATF6B (chr6p21.3) which encodes a transcription factor. Conclusions For the first time, our genome-wide methylation investigation found that residential PAH levels were associated with 11 CpGs at birth among children who later developed ALL. Moreover, the future cases had significantly different DNA methylation responses to PAH exposures than the unaffected controls for 7 CpGs. This may suggest a case/control difference present at birth in the sensitivity to PAHs in particular cell-cycle and tumor-suppressor genes. These CpGs may be good candidates to further investigate with respect to leukemogenesis. Citation Format: Semira Gonseth, Todd P. Whitehead, Ritu Roy, E. Andres Houseman, Adam J. de Smith, Mi Zhou, Seung-Tae Lee, Margaret R. Wrensch, Stephen M. Rappaport, Catherine Metayer, Joseph L. Wiemels. In utero polycyclic aromatic hydrocarbons exposure and genome-wide DNA methylation modifications at birth in children who develop acute lymphoblastic leukemia. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 831. doi:10.1158/1538-7445.AM2015-831

Human metabolic responses to chronic environmental polycyclic aromatic hydrocarbon exposure by a metabolomic approach.

The toxicities of polycyclic aromatic hydrocarbons (PAHs) have been extensively explored due to their carcinogenic and mutagenic potency; however, little is known about the metabolic responses to chronic environmental PAH exposure among the general population. In the present study, 566 healthy volunteers were dichotomized into exposed and control groups to investigate PAH-induced perturbations in the metabolic profiles. Nine urine PAH metabolites were measured by a sensitive LC-MS/MS method to comprehensively evaluate the PAH exposure level of each individual, and the metabolic profiles were characterized via a LC-MS-based metabolomic approach. PAH exposure was correlated to its metabolic outcomes by linear and logistic regression analyses. Metabolites related to amino acid, purine, lipid, and glucuronic acid metabolism were significantly changed in the exposed group. 1-Hydroxyphenanthrene and dodecadienylcarnitine have potential as sensitive and reliable biomarkers for PAH exposure and its metabolic outcomes, respectively, in the general population. These findings generally support the hypothesis that environmental PAH exposure causes oxidative stress-related effects in humans. The current study provides new insight into the early molecular events induced by PAH exposure in the actual environment.

Shrimp consumption after deepwater horizon: no evidence of excess risks for vietnamese americans.

Shrimp consumption after deepwater horizon: no evidence of excess risks for vietnamese americans.

Polycyclic Aromatic Hydrocarbons-Associated MicroRNAs and Their Interactions with the Environment: Influences on Oxidative DNA Damage and Lipid Peroxidation in Coke Oven Workers

We previously identified five polycyclic aromatic hydrocarbons (PAHs)-associated microRNAs (miRNAs) and found they were associated with chromosome damage. As oxidative damage is the common contributory cause of various PAHs-related diseases, we further investigated the influences of these miRNAs and their interactions with environmental factors on oxidative DNA damage and lipid peroxidation. We measured PAHs internal exposure biomarkers [urinary monohydroxy-PAHs (OH-PAHs) and plasma benzo[a]pyrene-r-7,t-8,t-9,c-10-tetrahydotetrol-albumin (BPDE-Alb) adducts], the expression levels of PAHs-associated plasma miRNAs (miR-24-3p, miR-27a-3p, miR-142-5p, miR-28-5p, and miR-150-5p), and urinary biomarkers of oxidative DNA damage [8-hydroxydeoxyguanosine (8-OH-dG)] and lipid peroxidation [8-iso-prostaglandin-F2α (8-iso-PGF2α)] in 365 healthy male coke oven workers. These miRNAs were associated with a dose-response increase in 8-OH-dG (β > 0), and with a dose-response decrease in 8-iso-PGF2α (β < 0), especially in workers with lower PAHs exposure levels, in nonsmokers, and in nondrinkers. These miRNAs interacted antagonistically with ΣOH-PAHs and BPDE-Alb adducts (βinteraction < 0) and synergistically with drinking status (βinteraction > 0) to influence 8-OH-dG, while they interacted synergistically with BPDE-Alb adducts (βinteraction > 0) and antagonistically with smoking status (βinteraction < 0) to influence 8-iso-PGF2α. Our results suggested that miRNAs and their interactions with environmental factors might be novel mechanisms mediating the effects of PAHs exposure on oxidative DNA damage and lipid peroxidation.

Personal inhalation exposure to polycyclic aromatic hydrocarbons in urban and rural residents in a typical northern city in China

Personal inhalation exposure samples were collected and analyzed for polycyclic aromatic hydrocarbons (PAHs) for 126 selected volunteers during heating and non-heating seasons in a typical northern Chinese city, Taiyuan. Measured personal PAH exposure levels for the urban residents in the heating and non-heating seasons were 690 (540-1051) and 404 (266-544) ng/m(3) , respectively, while, for the rural residents, they were 770 (504-1071) and 312 (201-412) ng/m(3) , respectively. Thus, rural residents are exposed to lower PAH contamination in comparison with the urban residents in the non-heating seasons. In the heating season, personal PAH inhalation exposure levels were comparable between the urban and rural residents, in part owing to the large rate of residential solid fuel consumption in the rural area for household cooking and heating. The estimated incremental lifetime cancer risks (ILCR) due to PAH exposure in Taiyuan were 3.36×10(-5) and 2.39×10(-5) for the rural and urban residents, respectively, significantly higher than the literature-reported national average level, suggesting an urgent need of PAH pollution control to protect human health.

Personal exposure levels of PAHs in the general population in northern rural area of Jiangsu Province, China

Polycyclic aromatic hydrocarbons (PAHs) are a group of compounds that are produced by incomplete combustion of organic matters. Studies in humans have shown associations between PAHs exposure and development of cancers. Urinary monohydroxy polycyclic aromatic hydrocarbons (OH-PAHs) are a class of PAH metabolites used as biomarkers for estimating human exposure to PAHs. We collected 332 urinary samples from a nonoccupational population in northern rural area of Jiangsu. Levels of 2-hydroxynathalene (2-OHN), 2-hydroxyfluorene (2-OHF) and 1-hydroxypyrene (1-OHP) were measured as biomarkers to assess body PAHs burdens. Three PAH metabolites were detected in more than 80% of urinary samples. After being adjusted with urinary creatinine concentration, the urinary concentrations were determined as 2-OHF > 1-OHP > 2-OHN in terms. The medians of 2-OHN, 2-OHF, 1-OHP for the general population were 1.74, 30.01, 25.24 μmoL/moL creatinine, respectively. The results demonstrated that nonoccupational populations in northern rural area of Jiangsu were exposed to extremely high PAHs. The urinary concentration (median and geometric mean) of 2-OHN,2-OHF,1-OHP in males (1.90, 0.37 ± 0.46; 34.90, 1.53 ± 0.41; 27.84, 1.52 ± 0.29 μmoL/moL creatinine, respectively) was slightly higher than in females (1.56, 0.32 ± 0.42; 29.60, 1.48 ± 0.40; 23.13, 1.49 ± 0.32 μmoL/moL creatinine, respectively). However, only 2-OHN was different significantly between males and females.

An analysis study of the exposure factors from an environmental hazardous material (1-hydroxyperene)

BACKGROUND Polycyclic aromatic hydrocarbons (PAHs) are composed more than two benzene rings that are formed by incomplete combustion of organic materials or the process of high-pressure. PAHs has potential carcinogenic and/or mutagenic properties. 1-Hydroxypyrene, the metabolite of pyrene, is used to assess the exposure of polycyclic aromatic hydrocarbons (PAHs). AIMS In this study, we analyzed the PAHs exposure levels of Korean adults participating to “Korean National Environmental Health Survey”, using the urinary 1-OHP levels as a biomarker for PAHs, and evaluated the exposure factors that closely associated with the level of urinary 1-OHP. METHODS We used log transformed urinary 1-OHP (log(1-OHP)) value as a dependent variable for analysis of the association with exposure factors. Multiple linear regression and logistic regression model were used to evaluate the relationship between log(1-OHP) and exposure factors. RESULTS In a multiple analysis, we observed that 1-OHP was significantly associated with variables including age group, education, smoke, drink, heating source, distance from the road, and charcoal grilled or roasted meet consumption. Results from multiple logistic regression analysis, we observed significant finding with variables including gender(male OR:1.53 (95% CI:1.02,2.31), education (above college OR:0.32 (95% CI:0.18,0.54) and smoke (current smoker OR:17.73 (95% CI:11.02,28.51). We evaluated the association between traffic related air pollution factors (use of public transportation, type of transportation and distance from the road) and log(1-OHP), however, only distance from the road was significantly associated with log(1-OHP) CONCLUSIONS The analysis shows that the factors, such as smoking habit, gender and charcoal grilled or roasted food consumption are significantly associated with log(1-OHP). These results may provide a supportive evidence of the finding from previous studies. These analysis results can be used as reference for policy making for reducing environmental hazardous materials.

Association between a biomarker of exposure to polycyclic aromatic hydrocarbons and semen quality

Growing evidence supports the reproductive and developmental toxicity of polycyclic aromatic hydrocarbons (PAHs) from prenatal and postnatal exposure, but the results of epidemiological studies regarding harmful effects of PAHs exposure on male reproductive system still remain limited and inconclusive. The aim of the present study was to investigate the relationship between 1-hydroxypyrene, a biomarker of polycyclic aromatic hydrocarbons exposure and semen quality. The study population consisted of 277 men attending an infertility clinic for diagnostic purposes and having normal semen concentration of 20-300 mln/ml or slight oligozoospermia (semen concentration: 15-20 mln/ml) (WHO 1999). All the men were healthy and under 45 years of age. All participants were interviewed and provided a semen sample. The interview included questions concerning demographics, socio-economic status, medical history related to past diseases which may have an impact on semen quality, lifestyle factors and occupational information. Concentrations of 1-hydroxypyrene (1-OHP) in the urine samples were analyzed using high performance liquid chromatography (HPLC). A positive association was found between the level of 1-OHP in urine and sperm neck abnormalities as well as the percentage of static sperm cells (p = 0.001, p = 0.018, respectively). Additionally, exposure to PAHs measured by 1-OHP in urine decreased semen volume and the percentage of motile sperm cells (p = 0.014, p = 0.0001, respectively). Presented findings indicate that the environmental level of PAHs exposure adversely affects male semen quality. The future large-scale studies should incorporate different biomarkers to generate a more accurate and full assessment of the effects of PAHs exposure on male fertility.

Health Risk Assessment of Polycyclic Aromatic Hydrocarbons (PAHs) in the Pearl River Delta

The objective of this study was to quantify PAHs exposure level for different resident groups and to estimate the incremental lifetime cancer risk for people in the Pearl River Delta. A multimedia/multipathway exposure model recommended by USEPA was employed in this study. Results indicated that the average cancer risk of exposure to PAH16 was 2.63×10-5 a-1 and the loss of life expectancy was 163.48 minutes. Considering the large amounts of PAHs emitted into the ambient environment in China and the loss of life expectancy, it is extremely important to take a preliminary health risk assessment of citizens exposed to PAHs in the Pearl River Delta.

Genetic variations of CYP2B6 gene were associated with plasma BPDE-Alb adducts and DNA damage levels in coke oven workers

Polycyclic aromatic hydrocarbons (PAHs), the main components of coke oven emissions, can induce activation of cytochrome P450 (CYP) enzymes, which metabolize PAHs and result in DNA damage by forming adducts. This study was designed to know whether genetic variants of CYP genes are associated with plasma benzo[a]pyrene-7,8-diol-9,10-epoxide-albumin (BPDE-Alb) adducts and DNA damage in coke oven workers. In this study, 298 workers were divided into four groups according to the environmental PAHs exposure levels. The concentrations of plasma BPDE-Alb adducts were detected by reverse-phase high-performance liquid chromatography and the DNA damage levels were measured using comet assay. Twelve tag single nucleotide polymorphisms (tagSNPs) of 4 CYP genes were selected and genotyped by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. In the top group, workers with CYP2B6 rs3760657GA genotype have lower BPDE-Alb adducts and DNA damage levels than those with rs3760657GG genotype (P<0.05). In the control group, the DNA damage levels of subjects with CYP1A1 rs4646421AA or GA+AA genotypes were lower than those with GG genotype (P<0.05). However, no such effects were shown for the other tagSNPs. These results suggested that genetic variations of CYP2B6 might be associated with low BPDE-Alb adducts and DNA damage levels in worker with high exposure to PAHs.

Biomarkers of exposure to polycyclic aromatic hydrocarbons (PAHs) and DNA damage: a cross-sectional pilot study among roofers in South Florida

ObjectiveThe main goal of this pilot study was to assess the technical and logistic feasibility of a future study. The research hypothesis is that occupational exposures to polycyclic aromatic hydrocarbons...

PREDICTORS OF ENVIRONMENTAL EXPOSURE TO POLYCYCLIC AROMATIC HYDROCARBONS AMONG PREGNANT WOMEN

Background and Aims: Polycyclic aromatic hydrocarbons (PAH) are a group of compounds, comprising two or more fused aromatic rings, that are formed as a result of incomplete combustion of organic matter. Sources of environmental contamination can be both industrial and nonindustrial, the most common sources being cigarette smoke, grilled and smoked food processes, coal-fired utilities, steel plants, coke-oven plants, graphite electrode manufacturing plants, vehicle exhaust, wood-burning ovens and fireplaces. The aim of the study was to characterize the PAH exposure level based on 1-hydroxypyrene (1-HP) in urine of Polish pregnant women. Methods: The study population consisted of 449 pregnant women who had been the subjects of the prospective Polish Mother and Child Cohort study performed in 8 regions of Poland. The women were interviewed three times during pregnancy (once in each trimester). 1–HP concentration in urine was chosen as the biomarker of exposure to PAH. The urine sample was analysed using high performance liquid chromatography (HPLC). The active and passive smoking exposure was verified by saliva cotinine, analysed by high performance liquid chromatography coupled with tandem mass spectrometry/positive electrospray ionisation (LC-ESI+ MS/MS) and isotope dilution method. Results: 1-HP concentration in urine ranged from 0.02 to 10.2 •g/g creatinine with the geometric mean (GM) 0.4 •g/g creatinine. The significantly higher concentration of urinary 1-HP in pregnant women was observed for summer collection (GM ratio 1.1; p = 0.01), among smokers (GM ratio 1.7; p &lt; 0.001) and for the women living in big cities (GM ratio 1.3; p = 0.001). Conclusions: The significantly higher concentration of urinary 1-HP in pregnant women was observed for summer collection, among smokers and those living in big cities.

Increase of urinary concentrations of 8-hydroxy-2′-deoxyguanosine in diesel exhaust emission inspector exposed to polycyclic aromatic hydrocarbons

The objectives of this study were to explore the factors influencing urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels in diesel engine exhaust emission inspectors (inspectors), the association between polycyclic aromatic hydrocarbons (PAHs) exposure and fine particulate matter (PM(2.5)) levels in diesel exhaust particles (DEPs), and the PAHs exposure levels in diesel vehicle emission inspection stations (inspection stations). Twenty-eight inspectors and a control group of thirty-eight individuals matched by age and gender were recruited for this study. Fifteen ambient air samples and eighty-four personal air samples were monitored during 3-day work periods using a repeated-measures study design in each inspection station. Airborne samples were analyzed with a fluorescence detector and by high-performance liquid chromatography. Urinary 8-OHdG was measured in 168 pre- and post-work urine samples from inspectors, and in 38 urine samples from controls. The concentrations of PAHs in DEP(2.5) (PM(2.5) in DEPs) were significantly and positively related to urinary log(10) 8-OHdG levels after adjusting for smoking status and BMI. Statistically, there was a significant correlation between air log(10) PAHs and air log(10) PM(2.5) concentrations in inspectors. Fifteen PAHs compounds within DEP(2.5) revealed the concentrations ranged from 5.18 to 22.93 ng/m(3) in ambient air monitoring and 1.03 to 12.60 ng/m(3) in personal air monitoring. This study is the first to indicate an association between occupational PAHs exposure from DEP(2.5) at an inspection station and an increased excretion of urinary 8-OHdG in inspectors. In addition, this study also found smoking is not a confounder in inspectors exposed to PAHs in DEP(2.5).

Quantification of carcinogenic 4- to 6-ring polycyclic aromatic hydrocarbons in human urine by solid-phase microextraction gas chromatography–isotope dilution mass spectrometry

Polycyclic aromatic hydrocarbons (PAHs) are pollutants found in living and working environments. The aim of this study was to develop a solid-phase microextraction (SPME) gas chromatography (GC)-isotope dilution mass spectrometry method for the quantification of 10 four- to six-ring PAHs in urine samples. Seven of the selected PAHs have been classified as carcinogenic. Under the final conditions, analytes were sampled with a 100-μm polydimethylsiloxane SPME fibre for 60 min at 80 °C and desorbed in the injection port of the GC at 270 °C. Fluoranthene, pyrene, benz[a]anthracene, chrysene, benzo[b]fluoranthene, benzo[k]fluoranthene, benzo[a]pyrene, dibenzo[a,h]anthracene, indeno[1,2,3-cd]pyrene and benzo[ghi]perylene were separated using a highly arylene-modified phase capillary column and quantified by MS using eight deuterated PAHs as surrogate internal standards. Limits of quantification (LOQ) were in the 0.5- to 2.2-ng/L range. Validation showed linear dynamic ranges up to 340 ng/L, inter- and intra-run precisions <20%, and accuracies within 20% of spiked concentrations. Matrix effect evaluation and the use of control charts to monitor process performances showed that the isotope dilution approach allowed for the control of bias sources. Urinary PAHs were above or equal to LOQ, depending on different compounds, in 58-100% (min-max), 40-100% and 5-39% of samples from coke oven workers (n = 12), asphalt workers (n = 10) and individuals not occupationally exposed to PAHs (n = 18), respectively. Chrysene was the most abundant PAH determined with median levels of 62.6, 6.9 and <0.6 ng/L, respectively. These results show that the method is suitable for quantifying carcinogenic PAHs in specimens from individuals with different levels of PAH exposure.