Effect of the Route of Administration on the Induction of Cytogenetic Damage and DNA Adducts in Peripheral Blood Lymphocytes of Rats and Mice by Polycyclic Aromatic Hydrocarbons

Experiments were designed to investigate how the route of exposure to polycyclic aromatic hydrocarbons (PAHs) in mice and rats affects the induction of cytogenetic end points and DNA adduction. Both mice and rats were exposed to 100 mg/kg of benz[ a ]anthracene (B[ a ]A), benzo[ b ]fluoranthene (B[ b ]F), benzo[ a ]pyrene (B[ a ]P), or chrysene (Chr) by gavage or by intraperitoneal injection (i.p.). Peripheral blood was removed by cardiac puncture 7 days after PAH administration. Blood samples were analyzed in parallel for sister chromatid exchange (SCE) frequency, the frequency of micronuclei in cytochalasin B-induced binucleate cells (MN bn ), and DNA adduction using 32P-postlabeling. The i.p. route of exposure produced both the highest levels of cytogenetic damage and DNA adducts for each PAH. The mouse was more sensitive than the rat to PAH exposure as measured by SCE induction and the total amount of DNA adducts/ w g DNA.     

DNA Adducts Derived from Diesel Emissions - Assessment of Genotoxic Potency in Vitro and Human Exposure Monitoring

Diesel particle extracts, which originated from three different diesel fuels, were used to study the activation of polycyclic aromatic hydrocarbons (PAHs). DNA adducts were analyzed in vitro calf thymus, human skin tissue culture and in lymphocytes isolated from diesel exposed workers. Direct-acting mutagens (e.g. nitro-PAHs) measured by Ames test were compared with DNA adducts formed in vitro by nitroreductive xanthine oxide enzyme. PAH-DNA adducts were analyzed by ³²P-postlabeling, and when characterizing adducts from skin DNA, a solid-phase micro extraction (SPME) method was developed for sample preparation before HPLC analysis. A good accordance between mutagenicity and DNA adducts showed that the three extracts contain higher amounts of direct-acting PAHs than the PAHs needing S9 activation. Skin DNA adducts demonstrated two-fold differences between the tissue cultures. ³²P-postlabeling and HPLC analysis did not confirm the identity of skin DNA adducts with the BPDE-DNA standard. The pilot study on 13 diesd exposed bus garage and waste collection workers showed low levels of PAH exposure (<50 ng/m³) and lymphocyte PAH-DNA adducts less than 2 adducts/10⁸ nucleotides.     

POLYCYCLIC AROMATIC HYDROCARBONS OF DIESEL AND GASOLINE EXHAUST AND DNA ADDUCT DETECTION IN CALF THYMUS DNA AND LYMPHOCYTE DNA OF WORKERS EXPOSED TO DIESEL EXHAUST

Particles present in urban air pollution are mainly derived from diesel- and gasoline-fueled vehicles. Exhaust emission is able to cause several health effects in humans including mutagenicity and carcinogenicity. Polycyclic aromatic hydrocarbons (PAHs) were measured in diesel and gasoline particulate extracts and DNA binding to CT DNA (±S9 and ±XO) was investigated. A large difference in content of 14 PAHs in diesel and gasoline extracts was observed, showing higher concentration of 14 PAHs, 6 carcinogenic PAHs, benzo[a]pyrene (B[a]P) in diesel than in gasoline extracts. Selected PAH standards of B[a]P, benzo[c]fluoranthene (B[c]F), and 3-nitrobenzanthrone (NBA) were used in ³²P-postlabeling/polyacrylamide gel electrophoresis (PAGE) technique to identify CT DNA adducts formed by diesel particulate extracts. CT DNA adduct formation was higher for diesel extracts in comparison with gasoline extracts; however, no clear origin of DNA adducts derived from B[c]F-, 3-NBA-, B[a]P was detected. ³²P-postlabeling/PAGE was a useful assay for analyzing and identifying PAH-DNA adducts. Occupational exposure to particulate and volatile PAH concentrations were evaluated using personal air samples and lymphocyte DNA adducts as markers of exposure. Overall air PAH concentrations were low in all eight workplaces, consisting of 97% of vapor phase compounds. DNA adducts analyzed by ³²P-postlabeling assay were compared between the butanol and nuclease P1 enrichment procedures. Only in winter samples of exposed workers, butanol extraction revealed significantly higher adduct levels in comparison with those of control persons. No differences in adduct levels between exposed and control persons in summer were detected by using either butanol extraction or nuclease P1 treatment. Total concentrations of particulate and volatile PAHs measured in eight workplaces in winter showed a significant correlation with total DNA adducts analyzed in workers' lymphocytes (r = 0.852N = 8, p = .007).     

THE RELATION BETWEEN BIOMARKERS AND OCCUPATIONAL EXPOSURE TO POLYCYCLIC AROMATIC COMPOUNDS

Recently a paper was published in which we reviewed a number of studies involving occupational surveys, where both the external polycyclic aromatic hydrocarbon (PAH) exposures and one or more biomarkers were quantitatively monitored. As part of that review a statistical analysis of the results of these studies was performed, which revealed that only urinary 1-hydroxypyrene (1OHPy) and possibly chromosome aberrations (CA) showed a correlation with PAH exposure, while unexpectedly, DNA adducts did not. Another observation was that although in controlled laboratory experiments good correlations have been found to occur between DNA adducts and exposure doses to polycyclic aromatic compounds (PACs), such a correlation was not found in the human occupational exposure studies reviewed. Also the analyses showed that sister chromatid exchanges (SCE) and micronuclei (MN) exhibited a very weak or an absence of a correlation, respectively, with external PAH exposure. The subject of this article is an attempt to explain: (a) why the levels of only some biomarkers correlate with PAH exposures and (b) the differences in results between controlled animal experiments and human monitoring studies.     

Characterization of PM2.5-Bound Polycyclic Aromatic Hydrocarbons in the Ambient Air of Győr,Hungary

ABSTRACT

In Hungary, the nationwide monitoring of PM10-bound polycyclic aromatic hydrocarbons (PAHs) in ambient air is great importance for a number of reasons related to human health, the environment and compliance with European Union legislation. However, the measurement of PAH concentrations in PM2.5 aerosol fraction has not been carried out. Therefore, the concentration, distribution and sources of PM2.5-bound PAHs at different urban sites of Gy?r were investigated in a heating season. The total PAH concentrations (sum of 19 individual PAH compounds) ranged from 1.32 to 37.27 ng/m³ with the mean value of 10.54 ng/m³. The high molecular weight PAHs with 5 and 6 aromatic rings were the most abundant PAHs in PM2.5 aerosol samples, which averaged 82% of total PAHs. Using benzo(a)pyrene (BaP) equivalent approach on the concentration data of carcinogenic PAH species, BaP and indeno(1,2,3-cd)pyrene contributed the highest carcinogenic exposure equivalent (1.25 and 0.19 ng/m³ on average). However, the incremental lifetime cancer risk (ILCR) values for resident children and adults indicated low-potential cancer risk (ILCR < 10^?6). The source apportionment results reflected that the major sources of PAH compounds in the Gy?r atmosphere were fossil fuel combustion and vehicle emissions.     

DNA Adducts Formed in vitro from Fractionated Extract of Urban Air Particles

This study is a part of an ongoing interdisciplinary project on the health effects of air pollution (Teplice Program) in the highly polluted district of Teplice, Northern Bohemia. In our previous studies we found the relationship between DNA adduct levels detected in white blood cells of selected Teplice population and personal exposure to PAH associated with respirable particles. In this pilot study we used ³²P-postlabeling assay for DNA adduct detection in an in vitro model system for evaluation of genotoxic activity of fractionated urban air extractable organic matter (EOM). To identify some of the specific DNA adducts formed we coupled TLC with HPLC analysis of labeled adducts. The urban air particles were collected by high-volume sampler during January-March 1992 in Teplice. EOM was extracted by dichlormethane (DCM) and crude extract was fractionated into five fractions to obtain a gross partition of different chemical classes. Fractions were incubated with calf thymus DNA (dose 100 μg/ml incubate) under oxidative and reductive conditions using two metabolic activation system: 1) an oxidative rat liver S9 system (S9) and 2) a reductive xanthine oxidase catalyzed system (XO). The different DNA adduct patterns and levels were determined using S9 and XO-mediated metabolism followed by postlabeling with both nuclease P1 and butanol extraction enrichment procedures for all fractions examined. The moderately polar fraction (DCM) contained over 50% of the total DNA adduct forming activity both without and with S9 activation. The highly polar fraction (methanol) contained about 60 % of the DNA adduct forming activity under reductive conditions. Some of the main distinct DNA adducts obtained with S9 and XO mediated metabolism were tentatively identified by HPLC comparing with standards of PAH- and nitro-PAH DNA adducts.     

Coal dust alters β-naphthoflavone-induced aryl hydrocarbon receptor nuclear translocation in alveolar type II cells

Background  

Many polycyclic aromatic hydrocarbons (PAHs) can cause DNA adducts and initiate carcinogenesis. Mixed exposures to coal dust (CD) and PAHs are common in occupational settings. In the CD and PAH-exposed lung, CD increases apoptosis and causes alveolar type II (AT-II) cell hyperplasia but reduces CYP1A1 induction. Inflammation, but not apoptosis, appears etiologically associated with reduced CYP1A1 induction in this mixed exposure model. Many AT-II cells in the CD-exposed lungs have no detectable CYP1A1 induction after PAH exposure. Although AT-II cells are a small subfraction of lung cells, they are believed to be a potential progenitor cell for some lung cancers. Because CYP1A1 is induced via ligand-mediated nuclear translocation of the aryl hydrocarbon receptor (AhR), we investigated the effect of CD on PAH-induced nuclear translocation of AhR in AT-II cells isolated from in vivo-exposed rats. Rats received CD or vehicle (saline) by intratracheal (IT) instillation. Three days before sacrifice, half of the rats in each group started daily intraperitoneal injections of the PAH, β-naphthoflavone (BNF).     

POLYCYCLIC AROMATIC HYDROCARBON REFERENCE RANGE LEVELS IN THE U.S. POPULATION BY MEASUREMENT OF URINARY MONOHYDROXY METABOLITES

We developed a gas chromatography/isotope dilution high- resolution mass spectrometry (GC/ID-HRMS) method for measuring 18 PAH metabolites representing 8 parent PAHs in 3 mL of urine at low part-per-trillion levels. We applied this method to the analysis of urine specimens from approximately 2400 people who participated in the National Health and Nutrition Examination Survey for the years 1999 and 2000 to determine levels for 14 PAH hydroxy metabolites of 7 parent compounds. Using this GC/ID-HRMS method, we found detectable concentrations for monohydroxy metabolite isomers of fluorene, phenanthrene, fluoranthene, and pyrene, and for chrysene, benzo[c]phenanthrene, and benz[a]anthracene. Some monohydroxy metabolite isomers of chrysene, benzo[c]phenanthrene, and benz[a]anthracene exhibited low detection frequencies which did not allow for geometric mean calculations. From our study, we established a reference range for the targeted PAHs in the general U.S. population.     

POLYCYCLIC AROMATIC HYDROCARBON REFERENCE RANGE LEVELS IN THE U.S. POPULATION BY MEASUREMENT OF URINARY MONO-HYDROXY METABOLITES

We developed a gas chromatography/ isotope dilution high resolution mass spectrometry (GC/ID-HRMS) method for measuring 18 PAH metabolites representing 8 parent PAHs in 3 mL of urine at low part-per-trillion levels. We applied this method to the analysis of urine specimens from approximately 2400 people who participated in the National Health and Nutrition Examination Survey for the years 1999 and 2000 to determine levels for 14 PAH hydroxy metabolites of 7 parent compounds. Using this GC/ID-HRMS method, we found detectable concentrations for monohydroxy metabolite isomers of fluorene, phenanthrene, fluoranthene, and pyrene, and for chrysene, benzo[c]phenanthrene, and benz[a]anthracene. Some mono-hydroxy metabolite isomers of chrysene, benzo[c]phenanthrene, and benz[a]anthracene exhibitedlow detection frequencies which did not allow for geometric mean calculations. From our study, we established a reference range for the targeted PAHs in the general U.S. population.     

THE SIGNIFICANCE OF POLYCYCLIC AROMATIC HYDROCARBONS AS ENVIRONMENTAL CARCINOGENS. 35 YEARS RESEARCH ON PAH—A RETROSPECTIVE

In vivo studies with laboratory animals as well as in vitro studies with bacteria and mammalian cell cultures have demonstrated that the mutagenic and/or carcinogenic properties of numerous PAHs require metabolic transformation. Metabolism of PAHs has been explored in vitro using cellular microsomal fractions, mammalian cell cultures and later genetically engineered cells expressing cytochromes P450 from several species including humans.

Balancing the carcinogenic potential of some environmental matrices (vehicle exhaust, condensate of hard coal combustion effluents, cigarette smoke condensate, used motor oil) after separation into sub-fractions evidenced that the carcinogenic effect may be attributed almost exclusively to PAH. Mixtures of well-known carcinogenic PAH in concentrations as present in these matrices, however, did not explain the total biological effect. Thus, it had been speculated that either very potent unknown carcinogens are still hidden in the PAH fraction, or that synergistic effects (enzyme induction) play a significant role.

In parallel to these carcinogenicity studies, the metabolism of various PAHs has been investigated in rat liver microsomes from untreated animals as well as from animals pre-treated with inducers of cytochrome P450. It was found that even non-carcinogenic PAHs possess a significant inducing potential. Moreover, in several mammals a highly species-specific metabolism of PAH could be observed allowing a critical view to the extrapolation from animal experiments to the human situation. This was further confirmed by experiments with mammalian cell cultures including human ones as well as by metabolic studies with genetically engineered Chinese hamster V79 cells singularly expressing various cytochrome P450 enzymes from a number of different species (human, rat, mouse, fish). With these cell lines metabolic studies were carried out with a larger number of PAHs as substrates including phenanthrene, pyrene, chrysene, benzo[a]anthracene, benzo[c]phenanthrene, benzo[a]pyrene, dibenzo[a,l]pyrene, and benzo[c]chrysene.

Based on the metabolism results, analytical methods have been developed to determine urinary biomarkers of human PAH exposure. Human biomonitoring studies have been performed with different occupationally exposed individuals as well as within smokers and non-smokers of the general population. Endogenous PAH exposure levels and changes in the urinary excreted metabolic profile depending on exposure level have been determined.     

Evaluation of PAH: DNA Adduct Formation in Rats Fed Coal Tar-Contaminated Diets

Previous studies have demonstrated that mouse lung is a target organ for the tumorigenic and genotoxic effects of coal tar. The present study evaluated PAH:DNA adduct formation in lung, liver, forestomach, and mammary gland of female CD rats fed various types of coal tar-contaminated diets. Coal tar-contaminated soil, an organic extract of contaminated soil, neat coal tar, and diets containing only B[ a ]P were evaluated. Ingestion of coal tar diets resulted in detectable levels of DNA adducts in lung and forestomach tissue. These adducts were primarily derived from benzo[ c ]fluorene and B[ a ]P. The adduct derived from benzo[ c ]fluorene was the most predominant. No adducts were detected in liver and mammary gland under the conditions employed in this study. The formation of a benzo[ c ]fluorene-derived DNA adduct in rat lung following coal tar exposure is consistent with previous studies performed with mice.     

Elimination of 1-Hydroxypyrene in the Urine of Workers from Different Workplaces as an Indicator of Occupational PAH Exposure

The exposure to PAH of 327 workers occupied at 12 different workplaces has been investigated. Beside conventional ambient monitoring 1-hydroxypyrene was determined in the urine of the employees. Our investigations show that at certain workplaces the internal exposure to PAH of the employees is inadmissibly high although the PAH air concentrations determined at most of the workplaces were below the current threshold limits. Workers from different work places have different 1-hydroxypyrene concentrations in urine. Even employees working at work places with comperable PAH concentrations in air eliminate different 1-hydroxypyrene concentrations in urine. Our results indicate that the determination of PAH in air is not sufficient for health surveillance. To ensure health surveillance a biological monitoring is necessary.     

The Effect of Local Cooking Methods on Polycyclic Aromatic Hydrocarbons (PAHs) Contents in Beef,Goat Meat,and Pork as Potential Sources of Human Exposure in Kisumu City,Kenya

Roasted meat is known to be a major source of human exposure to PAHs. The contribution of direct-heat charcoal-roasted, electric- oven grilled, and shallow-pan fried meat to human exposure in Kisumu City was not known although the three modes of cooking meat are very prevalent. This study analyzed the concentrations of the PAHs in raw beef, goat meat, and pork, investigated the effect of direct-heat charcoal roasting, electric-oven grilling, and shallow-pan frying on these concentrations, and compared their concentration levels with international standards for foods in order to assess the potential risks to consumers. Samples were taken from three popular meat-roasting hotels within Kisumu City, Kenya. Extraction of PAHs was done using liquid-liquid partition after saponification with alcoholic potassium hydroxide followed by clean-up on a silica gel column and final analysis by gas chromatography-mass spectrometry (GC-MS). Roasting and shallow-pan frying introduced new PAHs and significantly (P ≤ 0.05) increased the concentrations of those existing in raw meat. Direct-heat charcoal roast beef had 5 new PAHs and a total mean PAH content of 17.88 μg/kg, compared with a mean of 1.39 μg/kg for raw beef, with the potent dibenz(a,h)anthracene also being detected. Direct-heat charcoal roasted goat meat had three new PAHs and a total mean PAH content of 4.77 μg/kg, compared with a mean of 2.13 μg/kg in raw meat, with the potent benzo(a)pyrene concentration being 8.84% of the total mean PAH. Fried pork had 7 new PAHs and a total mean PAH content of 3.47 μg/kg, compared with a mean total of 0.17 μg/kg, detected in the raw meat. Roast beef had the highest individual PAH concentration (5.03 μg/kg) and highest total PAHs concentration (17.88 μg/kg), both being higher than acceptable EU limits. The PAHs from local raw and cooked meat were characterized and quantified for the first time in Kisumu City and the study therefore provided the needed baseline data on PAHs in raw and cooked meat.     

THE ROLE OF PAH-DNA ADDUCTS IN CAUSING CANCER

This article addresses the evidence for the mechanism of activation of polycyclic aromatic hydrocarbons (PAH) to “ultimate carcinogenic” DNA-binding metabolites in cells and describes how analysis of DNA adducts allowed the determination that the metabolites are dihydrodiol epoxides of PAH. Initially, the PAH-DNA adduct analysis techniques we developed allowed us to establish that the reactive form of PAH that bind to DNA in cells was not the K-region epoxide. Further development of PAH-DNA adduct analysis techniques allowed us to determine that in the case of the very potent carcinogen dibenzo[a,l]pyrene, the reactive metabolite was a diol epoxide with “fjord region” of the molecule. Collaborative studies of DNA adducts in cells from a mouse in which cytochrome P450 1B1 levels were knocked out demonstrated that DB[a,l]P activation to DNA binding intermediates was reduced to undetectable levels demonstrating the great importance of this enzyme in activating fjord region containing PAH.     

Validation of Bioassays for Assessing the Contamination of Marine Environments

Various biomarkers were used to determine the exposure of fish (Arius felis and Micropogon undulatus) from Galveston Bay (GB), Texas, USA to organic contaminants. Sediment levels of polynuclear aromatic hydrocarbons (PAHs) in GB ranged from 81 to >1000 ng/g and polychlorinated biphenyls (PCBs) were <20 ng/g at all stations. No significant differences in hepatic concentrations of contaminants and ethoxyresorufin O–deethylase (EROD) activity, CYPIA mRNA levels, and DNA adducts were found in A. felis from GB. However, significant differences in biliary concentrations of naphthalene, phenanthrene, and benzo[a]pyrene metabolites were observed. Induced EROD activities and elevated levels of biliary PAH metabolites were measured in M. undulatus from the two most contaminated sites in GB. Induction toxic equivalents (I-TEQs), derived from dosing rat hepatoma H4IIE cells with hepatic extracts of A. felis, were correlated with tissue levels of ≥4–ring PAHs.     

Revealing the Origin of Polycyclic Aromatic Hydrocarbons in an Urban Snowpack

Polyciclic aromatic hydrocarbons (PAHs) are ubiquitous pollutants in urban atmosphere. Several PAHs are known carcinogens or are the precursors to carcinogenic daughter compounds. Understanding the contributions of various PAH emission sources is critical to appropriately managing PAH levels in the environment. The sources of PAHs to urban snowpack in Shelekhov city, Eastern Siberia, characterized by extremely high levels of PAH accumulation in snow were determined by using end-member mixing approach. The best potential to distinguish PAH emission sources is exhibited by ratios of PAH pairs of the principal mass 228, 252, and 276. The ratios of PAH pairs were used as tracers of end-member PAH sources. The contributions of sources were calculated using systems of linear equations. The results obtained using ratios of PAH pairs were compared with those obtained using molecular diagnostic ratios. It was shown that the results obtained using diagnostic ratios as tracers are less reliable than the results obtained using the ratios of the sums of PAHs.     

Organ Specific Distribution of PAHs in a Carnivorous Fish Species Following Chronic Exposure to Used Synthetic-Based Drilling Mud

The rapid growth of offshore oil and gas exploration on the Western Indian Continental shelf has generated the need for both general and region-specific scientific information on the environmental consequences of drilling activities. Much of the toxicity related to drilling mud discharges has been attributed to Polycyclic Aromatic Hydrocarbons (PAH) content. This study addressed concerns related to the potential for contamination and subsequent bioaccumulation of PAHs in Oreochromis Mossambicus from the disposal of used synthetic-based drilling mud (SBM). The LC₅₀, 96 h for solid phase and suspended particulate liquid phase, was 37,550 mg/L and 40,390 mg/L, respectively, which was within the acceptable limits as per the Ministry of Environment and Forests (MoEF) Notification, New Delhi, dated August 30, 2005. After chronic exposure (for 55 days) to used SBM, higher mean values of PAHs accumulation were obtained from the Tilapias exposed to higher SBM concentration. The highest level of accumulation was noted for Naphthalenes and the lowest for Benzo (a) pyrenes. Liver was the primary organ for PAH accumulation, while least was observed in muscle. From the observations made on PAH levels in control as well as exposed fish, we found SBM concentration dependant bioaccumulation, suggesting the potential high risk of PAH toxicity to the fish inhabiting in the vicinity of disposal site.     

Removal of polyaromatic hydrocarbons from scrap tires by solvent extraction

This study analyzes polycyclic aromatic hydrocarbon (PAH) compounds released from scrap tires by GC/MS and introduces a simple extraction process at ambient conditions to remove PAHs from scrap tires. The PAH species released from scrap tires included seven PAH compounds with high molecular weight and 4- and 5-aromatic rings and total-PAH content of 159 mg/L. When scrap tires were extracted using hot water (180 °C) for 3 h, the overall removal efficiency was 53%, indicating that PAHs were not adequately removed by this method. However, using organic solvents, the overall PAH removal efficiency improved to 82% for propionic acid and 70% for acetic acid, because the mass transfer of PAHs within scrap tires increases with decreasing dielectric constant. The PAH removal efficiency was dependent on solvent type and temperature.     

Beyond 16 Priority Pollutant PAHs: A Review of PACs used in Environmental Forensic Chemistry

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous in soils and sediments, particularly in urbanized environments in which the concentrations of 16 (or so) PAHs are regulated. Distinguishing among the numerous PAH sources is of practical and legal concern and thereby is often an objective of environmental forensic chemistry studies. Studies of prospective sources and impacted soils and sediments that rely upon the 16 U.S. EPA Priority Pollutant PAHs are disadvantaged, as these few compounds generally lack the specificity to distinguish among different PAH sources in the environment. Advances in analytical and interpretive methods over several decades have shown that different PAH sources can be more defensibly distinguished using modified EPA Method 8270 that, among other improvements, measure many other polycyclic aromatic compounds (PACs) that co-occur with the Priority Pollutant PAHs in different sources and in the environment. The PACs include variously-alkylated PAHs and polycyclic aromatic sulfur heterocyclics (PASHs) homologs and individual isomers, which are herein reviewed. Collectively, these PACs provide a higher degree of specificity among PAC sources and can be used to understand the effects of weathering on PAH assemblages. Despite their diagnostic capacity, PACs should not be relied upon at the exclusion of other compound groups (e.g., petroleum biomarkers) in most environmental forensic chemistry studies. In light of these advances, source characterization studies that rely only upon the 16 (or so) Priority Pollutant PAHs warrant considerable caution.     

Personal Exposure of Children to Particle-Associated Polycyclic Aromatic Hydrocarbons in Tianjin,China

Polycyclic aromatic hydrocarbons (PAHs) associated with fine particles are harmful to human health, particularly to children, who are most vulnerable. To evaluate the respiratory exposure of children to particle-associated PAHs properly, personal air sampling near breathing zone of 36 schoolchildren were conducted in Tianjin, China. Sixteen priority PAHs designated by the United States Environmental Protection Agency were measured using GC-MS. The average concentrations of personal exposure to ∑₁₆PAH were 27.31 ± 3.91 ng/m³ in summer and 58.18 ± 24.68 ng/m³ in winter. Moreover, PAH profiles were studied and the results showed NAP, BbF, and IPY were the most abundant PAHs. Five rings PAH species made up the largest proportion, accounting for 25.7% in summer and 32.6% in winter. Diagnostic ratios and principal component analysis indicated combustion activities were the major source for children exposure to particle-associated PAHs in this study. According to the risk assessment results, the inhalation exposure risk for children were higher than the acceptable risk level of 10–⁶, indicating the health issues of children should be paid more attention. On the basis of sensitivity analysis results, further research should be done to improve the inhalation cancer slope factor of BaP and the concentration distribution of PAHs in order to improve the accuracy of the health risk assessment.