PAH Exposure Research Articles

The influence of demographic and lifestyle factors on urinary levels of PAH metabolites-empirical analyses of Cycle 2 (2009-2011) CHMS data.

Polycyclic aromatic hydrocarbons (PAHs) are a group of compounds formed during the incomplete combustion of organic matter. Several are mutagenic carcinogens; the magnitude of exposure can be assessed by examining urinary levels of PAH metabolites. Data from biomonitoring studies that record urinary PAH metabolite levels, as well as demographic and lifestyle information, can be used to investigate relationships between PAH exposure and variables, such as smoking status, workplace smoking restrictions, age, sex, household income, home age, and occupation. This study analysed creatinine-adjusted urinary PAH metabolite concentrations and questionnaire data from ~1200 individuals aged 16 years and older surveyed in Cycle 2 of the Canadian Health Measures Survey (CHMS). Statistical analyses revealed that smoking status, age, and sex are associated with urinary concentrations of a pyrene metabolite (1-OHP), phenanthrene metabolites (ΣOH-Phen), fluorene metabolites (ΣOH-Flu) and naphthalene metabolites (ΣOH-Nap). More specifically, smoking status, age and sex can collectively account for 30, 24, 52, and 34% of the observed variations in 1-OHP, ΣOH-Phen, ΣOH-Flu and ΣOH-Nap metabolites, respectively (p < 0.001). Analyses of non-smokers revealed weak but significant effects of age, sex, home age, and occupation on urinary levels of selected PAH metabolites (i.e., <7% of observed variation, p < 0.05). The unexplained variation in PAH metabolite levels is most likely related to diet, which was not examined. Although the results revealed significant relationships between urinary PAH metabolite levels and several lifestyle and/or demographic variables, robust examinations of selected effects (e.g., sex, home age, occupation) will require datasets that are balanced with respect to the other highlighted variables. The results can be used to identify remedial measures to reduce exposure and concomitant risk, and/or design follow-up studies to test hypotheses regarding the causes of exposure differences empirically related to sex, age, home age, and occupation.

Towards a recommended biomonitoring strategy for assessing the occupational exposure of roofers to PAHs

The aims of this work were to assess the PAH exposure among roofers and to identify relevant biomarkers for monitoring occupational exposure. Several campaigns were conducted between 2004 and 2017, with 28 individual air samples and 240 urinary samples collected from 73 roofers. Seventeen parent PAHs and 14 urinary biomarkers, metabolites of pyrene (1-OHP), benzo(a)pyrene (3-OHBaP and TetraolBaP), naphthalene (1- and 2-naphtols), fluorene (1- 2- 3- 9-fluorenols) and phenanthrene (1- 2- 3- 4- 9-phenanthrols), were analysed. Three exposure groups were considered: soft-applied roofing using polymer-modified bitumen ("PMB"), hot-applied roofing using oxidized bitumen ("OB") and the tearing off of old roof coatings containing coal tar ("CT"). The PAHs containing 2–3 rings were much more abundant, and the highest airborne levels were observed in the "CT" group. The biomonitoring results were consistent with these results, with a large predominance of 2–3 ring PAH metabolites. 1-OHP, 3-fluorenol and 2-phenanthrol were better correlated with airborne levels and less influenced by smoking than the other metabolites. Conversely, 1-/2-naphtol levels were heavily influenced by smoking and not correlated with airborne naphthalene levels. Moreover, 3-OHBaP and TetraolBaP levels were very low when applying bitumen membranes, and much higher exposures were observed during tear-off activities. In this context, the recommended strategy for roofer biomonitoring should include 1-OHP, fluorenols and phenanthrols, as well as carcinogenic BaP metabolites (3-OHBaP or TetraolBaP) when evaluating the occupational exposure of roofers that are tearing off old roof coatings.

The interaction effects of smoking and polycyclic aromatic hydrocarbons exposure on the prevalence of metabolic syndrome in coke oven workers

IntroductionMetabolic syndrome (MetS) is a cluster of interrelated risk factors, which increase the risk of cardiovascular disease (CVD) and cancer. The prevalence of MetS might be affected by environmental pollution and individual’s poor lifestyles. MethodsIn this cross-sectional study, we aimed to evaluate the interactions effect of PAHs exposure and poor lifestyles on MetS among coke oven workers. We measured the concentrations of 11 urinary PAH metabolites among 682 coke oven workers by HPLC-MS. China adult blood lipid abnormality prevention guide (2016) was employed for diagnosing MetS. An interaction effect was tested in the modified Poisson regression models. ResultsThe results showed that the urinary level of 1-NAP (P for trend = 0.043) and 2-FLU (P for trend = 0.037) had significant dose-response relationships with increased PR of MetS. For 1-NAP, statistically significant positive association was with low HDL among individuals (P for trend = 0.003). Besides, smoking was associated with a significantly increased risk of prevalence ratio of MetS (PR = 1.07; 95% CI 1.00–1.13), high triglycerides (PR = 1.13; 95% CI 1.05–1.20) and low HDL (PR = 1.07; 95% CI 1.01–1.14). Smokers who with high levels of 1-NAP and 2-FLU had higher prevalence ratio of MetS compared with non-smokers who with low levels of 1-NAP [PR (95% CI): 1.17 (1.06–1.29); P for trend = 0.002] and 2-FLU [PR (95% CI): 1.17 (1.06–1.29); P for trend = 0.004]. ConclusionsOur findings suggested PAHs exposure increased the prevalence ratio of MetS and this effect can be modified by smoking status.

Analysis of urinary metabolites of polycyclic aromatic hydrocarbons and cotinine in pooled urine samples to determine the exposure to PAHs in an Australian population.

Our previous biomonitoring study of hydroxylated polycyclic aromatic hydrocarbons (OH-PAHs) in a population in Australia found high levels of 1-naphthol, a metabolite of both naphthalene and carbaryl, in some adult samples. Here, we conducted a follow-up study to collect and analyse pooled urine samples, stratified by age and sex, from 2014 to 2017 using a GC-MS method. Geometric mean concentrations of 1-hydroxypyrene, the most common biomarker of PAH exposure, were 100 and 120 ng/L urine in 2014–2015 and 2016–2017, respectively. The concentrations of most OH-PAHs in this study except 1-naphthol are in line with those reported by biomonitoring programs in the US and Canada. In general, concentrations of OH-PAHs are lower in samples from small children (0–4 years) and school-aged children (5–14 years) compared with samples from the older age groups, except for some cases in the recent monitoring period. The concentrations of 1-naphthol in some adult samples of both sexes are very high, which is consistent with our previous findings. Such high concentrations of 1-naphthol together with the high 1-naphthol/2-naphthol ratio suggest potential exposure to the insecticide carbaryl in this population but other exposure sources and different rates of naphthalene metabolism should also be investigated.

Association between a urinary biomarker for exposure to PAH and blood level of the acute phase protein serum amyloid A in coke oven workers

BackgroundCoke oven workers are exposed to both free and particle bound PAH. Through this exposure, the workers may be at increased risk of cardiovascular diseases. Systemic levels of acute phase response proteins have been linked to cardiovascular disease in epidemiological studies, suggesting it as a marker of these conditions. The aim of this study was to assess whether there was association between PAH exposure and the blood level of the acute phase inflammatory response marker serum amyloid A (SAA) in coke oven workers.MethodsA total of 87 male Polish coke oven workers from two different plants comprised the study population. Exposure was assessed by means of the individual post-shift urinary excretion of 1-hydroxypyrene, as internal dose of short-term PAH exposure, and by anti-benzo[a]pyrene diolepoxide (anti-B[a]PDE)-DNA), as a biomarker of long-term PAH exposure. Blood levels of acute phase proteins SAA and CRP were measured by immunoassay. C-reactive protein (CRP) levels were included to adjust for baseline levels of SAA.ResultsMultiple linear regression showed that the major determinants of increased SAA levels were urinary 1-hydroxypyrene (beta = 0.56, p = 0.030) and serum CRP levels (beta = 7.08; p < 0.0001) whereas anti-B[a]PDE-DNA, the GSTM1 detoxifying genotype, diet, and smoking were not associated with SAA levels.ConclusionsUrinary 1-hydroxypyrene as biomarker of short-term PAH exposure and serum levels of CRP were predictive of serum levels of SAA in coke oven workers. Our data suggest that exposure of coke oven workers to PAH can lead to increased systemic acute response and therefore potentially increased risk of cardiovascular disease.

Polycyclic aromatic hydrocarbons exposure and hematotoxicity in occupational population: A two-year follow-up study

BackgroundPolycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental and occupational pollutants. To date, the effect and mechanism by which PAHs exposure impaired hematopoietic system remains unclear. MethodsWe examined the capability of PAHs to disrupt hematopoiesis in a study of 639 male participants in China by measuring complete blood counts (CBC) in 2013 and 2014. Gas chromatography–mass spectrometry (GC/MS) method was used to measure airborne levels of PAHs and benzene. We measured 1-hydroxypyrene (1-OHP), S-phenylmercapturic acid (SPMA) and 8-hydroxy-2′-deoxyguanosine (8-OHdG) in urinary by ultra-high performance liquid chromatography-mass spectrometry (UPLC-MS/MS) method. ResultsWe found decreased dose−response of white blood cells, eosinophils, monocytes and lymphocytes with increased PAHs exposure in two consecutive years. We did not find association between benzene with CBC in our study. After stratification analysis by smoking status, the findings were highly consistent. White blood cells, monocytes and red blood cell counts were decreased in high urinary 8-OHdG group. ConclusionsOur study showed that PAHs could impair the hematopoietic system independently, and oxidative stress might play an important role in potential hematotoxicity.

A Rapid and Sensitive Method of Determination of 1-Hydroxypyrene Glucuronide in Urine by UPLC–FLD

A simple and sensitive method for analysis of 1-OHP-G in urine to evaluate PAHs exposure was established. The urine was extracted with a OASIS PRiME HLB column, and the eluent was directly injected into HPLC–FLD for analysis. The separation was carried out on a ACQUIIY UPLC BEH C18 column (2.1 × 50 mm, 1.7 μm), using methanol–1.5% formic acid water (60:40, v:v) as mobile phase at the flow rate of 0.2 mL/min. 1-OHP-G was detected at the excitation wavelength of 338 nm and the emission wavelength of 379 nm. Good linearity was obtained from 0.010 to 5.0 ng/mL for 1-OHP-G. The limit of detection of 1-OHP-G was 0.0032 ng/mL and the limit of quantification was 0.010 ng/mL. The intra-day and the inter-day precisions were 1.68, 4.98 and 1.81%, 5.00% at the concentrations of 0.010 ng/mL and 5.0 ng/mL, respectively. The proposed method was applied for urine sample analysis and the whole procedure could be completed within 8 min with the recoveries of 91.9–109%, 92.7–107% and 94.5–107% at the concentrations of 0.010 ng/mL, 1.0 ng/mL and 5.0 ng/mL, respectively. The results of 41 urine samples from non-professionals measured with the proposed method and UPLC–MS/MS were compared by Bland–Altman test and Passing–Bablok regression, showing a good agreement between the two methods. Moreover, dynamic change of urinary 1-OHP-G after eating barbecued food was detected by the proposed method and the results were consistent with the reported researches about 1-OHP. The proposed method was simple and rapid, and it could also to meet the assessment of population exposure to PAHs with high sensitivity and accuracy.

Deepwater Horizon crude oil exposure alters cholesterol biosynthesis with implications for developmental cardiotoxicity in larval mahi-mahi (Coryphaena hippurus)

During the spring and summer of 2010, the Deepwater Horizon (DWH) oil well released over three million barrels of crude oil into the Gulf of Mexico. As the oil dispersed it contaminated ecosystems that support numerous Gulf species including mahi-mahi (Coryphaena hippurus). The timing of the spill, and location of the surface slick, coincided with the spawning of many species in the region, raising concerns over embryonic and larval exposure. Numerous abnormalities due to crude oil exposure have been documented in fish early life stages, including cardiotoxicity; however, knowledge of the molecular mechanisms that cause these phenotypes is still limited. Several transcriptomic studies have presented cholesterol biosynthesis as one of the top enriched pathways following PAH exposure. In this study we exposed mahi-mahi embryos to DWH oil collected from the surface slick. At exposures ranging from ∑PAH 1.69 μg/L to ∑PAH 5.99 μg/L, the resulting larvae demonstrated significant increases in farnesyl-diphosphate farnesyltransferase 1 (fdft1) and an upward trend in 3-Hydroxy-3-Methylglutaryl-CoA Reductase (hmgcr) expression, genes that encode key enzymes in the cholesterol biosynthetic pathway. In addition to the increased expression of genes in cholesterol biosynthetic pathway, a significant decrease in total cholesterol was observed in larval homogenates, at ∑PAH 8.3 μg/L. These data confirm earlier transcriptomic studies and show that oil may diminish cholesterol and adversely impact numerous cellular functions due to altered membrane stability.

Biomonitoring of children exposure to urban pollution and environmental tobacco smoke with hair analysis – A pilot study on children living in Paris and Yeu Island, France

The impact of pollution on children's health has been increasingly pointed out in numerous studies which emphasized their increased vulnerability compared to adults. This pilot study investigated the relevance of hair analysis for the assessment of children exposure to pollution and to environmental tobacco smoke (ETS). The methodology based on GC–MS/MS and LC-MS/MS, is the first one to investigate simultaneously parent PAH (n = 15), PAH metabolites (n = 56), nicotine and cotinine in a biological matrix. The method was applied to hair samples collected from 25 children, aged from 2 to 11 years, living in Paris, France, selected as densely populated area with urban pollution including vehicle exhausts, and Yeu Island, a French island in the Atlantic ocean, selected as control area with low population density and no fuel powered vehicles. Nicotine and cotinine were detected in all the samples at concentrations up to 2275 pg/mg and 110 pg/mg respectively, suggesting exposure to ETS in the two areas. 10 parent PAH and 10 metabolites were detected in 100% and in >90% of the samples respectively. Eight of these biomarkers presented a significantly higher concentration in children from Paris than from Yeu Island. The results suggest association between PAH exposure and estimated time of exposure to vehicle exhaust as well as higher exposure to both PAH and ETS in the youngest children. Although these findings need to be confirmed on wider populations, the results obtained in this pilot study strongly support the relevance of hair analysis for the biomonitoring of children exposure to urban pollution and ETS.

Association between PAHs biomarkers and kidney injury biomarkers among kitchen workers with microalbuminuria: A cross-sectional pilot study

To study the association between kidney injury biomarkers and urinary OH-PAH metabolites in kitchen workers, with microalbuminuria. A cross-sectional pilot study was conducted among 120 male kitchen workers in a mega kitchen located at Coimbatore, India. Personal and sub-clinical details of study subjects were collected using a questionnaire. Albumin, creatinine, and albumin-creatinine ratio (ACR) were measured using urine dipstick test for the determination of microalbuminuria. Urinary hydroxylated PAHs metabolites (1-NAP, 9-HF, 3-HF, 2-HF, 9-PHN, and 1-OHP) were measured using GC-MS/MS and urinary kidney biomarkers (uNGAL, uCyst-C, uKIM-1, uOPN, and uTIMP-1) were measured using Multiplex Reader. Concentrations of urinary PAHs metabolites (1-NAP, 3-HF, 2-HF, 9-PHN, and 1-OHP) and kidney biomarkers (uKIM-1, uTIMP-1, uCyst-C and uNGAL) were significantly higher among kitchen workers with MAU compared to non-kitchen workers with MAU. Urinary kidney biomarkers viz., uKIM-1, uTIMP-1, uCyst-C, uNGAL, and uOPN showed higher median concentration among the kitchen workers with MAU compared to kitchen workers without MAU. Significant positive correlation was observed for 9-HF with uKIM-1 and uTIMP-1 and 1-OHP with uKIM-1. ACR was also well correlated with urinary kidney biomarkers. ROC analysis showed higher sensitivity and specificity for uKIM-1, uCyst-C, and uNGAL as biomarkers for early prediction of acute kidney injury among kitchen workers. The PAHs exposure among kitchen workers can lead to kidney injury. This was evident from the association of OH-PAHs and kidney injury biomarkers in kitchen workers with microalbuminuria.

Identifying Prenatal PAH Exposure and DNA Methylation Changes in Cord Blood Using a Novel Analytic Approach

PAH are ubiquitous in the urban environment, generated by combustion processes. Ambient PAH penetrate into the indoor environment. The CCCEH cohort study in NYC, a participant in the NIH ECHO conso...

Polyaromatic Hydrocarbons Depositions and Their Carcinogenic Risk Assessment in the Foundry Workers

The study was initiated to determinants of inhalation exposure to polycyclic aromatic hydrocarbon compounds (PAHs) among iron foundry workers in different workplace namely, molding, melting, shaking, blasting and finishing sections. The study population included five sections of foundry workers: 22 molding, 25 melting, 20 shaking, 18 blasting and 15 finishing workers. During work shifts, personal air samples were collected from each worker’s breathing zone using a PTFE filter and cassette holder connected in series with an XAD-2 sorbent tube. The entire sample were analysed for sixteen PAHs with HPLC. The total inhalation exposure of total PAHs (ΣPAHs) concentrations was 46.64 μg/m3 ranging 0.08–478.43 μg/m3 in all the samples. The PAHs with lower molecular weight and higher molecular weight contributed 55.02% and 44.98%, respectively, to the ΣPAHs. About 16% exposure samples collected at various sections of foundry exceeded the PAHs level prescribed by NIOSH standard limit. The highest level of ΣPAHs were found in the molding (82.64 μg/m3) followed by finishing (67.86 μg/m3), blasting (34.74 μg/m3), shaking (25.04 μg/m3) and melting (23.48 μg/m3) sections, respectively. By applying risk assessment it was estimated that the total unit risk of PAHs harming the foundry workers was 9.43 × 10–4 and about 95% of total risk is contributed by benzo[α]pyrene (BaP) and dibenzo [α h]anthracene (DahA). The study indicating the inhalation risk due to these PAHs exposures are not negligible and should be taken into account for health protection of the workers to address the quantitative aspects relating lung cancer risks to PAHs compounds in foundries.

Abstract 4327: The epigenetic effects of benzo[a]pyrene exposure

Abstract Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental carcinogens formed from the incomplete combustion of organic materials. Exposure to PAHs can be linked to at least 9 different cancer types, including lung and breast cancer. PAH are genotoxic and can form DNA adducts which can either be repaired or lead to mutations. DNA repair can lead to aberrant DNA methylation, however, few studies have investigated the link between PAH exposure and DNA methylation modifications. Here, we have used a mouse model to investigate the epigenetic consequences of PAH exposure. Mice (n=3/group) were treated by oral gavage with 0, 25, 50 and 75 mg/kg bodyweight/day of benzo[a]pyrene (BaP) for 28 days. Lung DNA from these mice was used to prepare Reduced Representation Bisulphite Sequencing (RRBS) libraries which were then sequenced using Illumina HiSeq2500to an average depth of 25x. For each mouse, DNA methylation was averaged over 500 bp tiled windows and differentially methylated regions (DMRs) were identified by comparing the controls (untreated) with all BaP-exposed mice (treated) irrespective of dose. In the treated vs untreated we identified 1815 windows (&amp;gt;25% methylation difference, p&amp;lt;0.05). Of these, we found that DMRs were under-represented in 5' untranslated regions (UTR), promoter, long interspersed nuclear elements (LINEs) regions and CpG islands compared with the genomic distribution of windows. DMRs were found to occur significantly more frequently in transcription termination regions. In addition, we found significantly more hypomethylation events in exon, intergenic, intronic and promoter regions, long terminal repeats (LTR) and short interspersed nuclear elements (SINE) and more hypermethylation in LINEs. Pyrosequencing validation on a selection of these DMRs is ongoing, using DNA from the same mice used in RRBS, plus mice exposed to BaP and other PAHs in lung and other tissues. In summary, these results show that PAHs have an effect on DNA methylation, and that these changes happen mostly within the gene body or intergenically, with significantly less differences observed at traditional gene expression regulators such as promoters. This implies that the DNA methylation changes effected by BaP exposure may serve another purpose other than gene expression regulation. Citation Format: Francesca Galea, Paul A. White, Volker M. Arlt, Paolo Vineis, James M. Flanagan. The epigenetic effects of benzo[a]pyrene exposure [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 4327.

Environmental and lifestyle factors affecting exposure to polycyclic aromatic hydrocarbons in the general population in a Middle Eastern area

The aim of this study was to investigate environmental and lifestyle factors affecting exposure to PAHs in the general population in a large city of the Middle East (Tehran) by measuring urinary monohydroxy polycyclic aromatic hydrocarbons (OH-PAHs) and establishing relationships between PAHs exposure and related factors. Urine samples were collected from 222 randomly chosen subjects who were living in the urban area of Tehran, Iran. Subjects were required to complete a detailed questionnaire aimed to document their personal and sociodemographic information, activities, cooking-related appliances, smoking history/exposure, and consumed foodstuff. Identification and quantification of six OH-PAHs was carried out using a gas chromatography with mass spectrometry (GC-MS). The geometric means for 1-OHP, 1-NAP, 2-NAP, 2-FLU, 9-FLU, and 9-PHE for whole population study were 310, 1220, 3070, 530, 330, and 130 ng/g creatinine, respectively. The two naphthalene metabolites contributed on average 77% of the total concentration of six measured OH-PAHs, followed by the 2-FLU, 1-OHP, 9-FLU, and 9-PHE. The most important predictors of urinary PAHs were consumption of grilled/barbecued foods, smoking, and exposure to environmental tobacco smoking. Water pipe smoking was linked to urinary OH-PAH metabolite in a dose-response function. Residential traffic was also related with OH-PAH metabolite concentrations. Other factors including gender, age, exposure to common house insecticides, open burning, and candle burning were found to be statistically associated with the urinary levels of some OH-PAHs. High exposure to PAHs among general population in Middle Eastern large cities and its associated health implications calls for public health measures to reduce PAHs exposure.

Relationship between residence characteristics and polycyclic aromatic hydrocarbon exposure in housewives: second Korean National Environmental Health Survey (2012\u20132014)

BackgroundPolycyclic aromatic hydrocarbons (PAHs) produced by incomplete combustion have negative effects on human health due to their carcinogenicity and teratogenicity. Indoor sources of PAHs include tobacco smoke, heating sources, and cooking. This study evaluated the relationship between human PAH exposure and residence characteristics.MethodThis study was based on the second Korean National Environmental Health Survey (2012–2014). Non-smoking housewives were included in the analyses (n = 1269). The concentrations of urinary PAH metabolites (2-naphthol, 2-hydroxyfluorene, 1-hydroxyphenanthrene, and 1-hydroxypyrene) were adjusted by urine creatinine level. The geometric mean concentrations of urinary PAH metabolites by residential factors were examined. Logistic regression models were used to evaluate associations between residential variables and PAH exposures.ResultsThe adjusted geometric mean concentrations of urinary 2-hydroxyfluorene and 1-hydroxyphenanthrene were significantly higher in the group residing within 100 m of a major road (p < 0.05) than in those residing > 100 m from a major road. In logistic regression analyses, the odds ratio (OR) for exceeding the third quartile of urinary 1-hydroxypyrene concentration was significantly higher in the group using coal or wood fuel for residential heating than in the group using gas (OR = 2.745, 95% confidence interval [CI] = 1.295–5.819). The detached house group had a significantly higher OR for 1-hydroxyphenanthrene compared with the apartment group (OR = 1.515, 95% CI = 1.023–2.243).ConclusionOur study shows the evidence of associations between some urinary PAH metabolite levels (1-hydroxyphenanthrene and 1-hydroxypyrene) and residence characteristics. Additional studies are needed to clarify these associations.

Phototoxic effects of PAH and UVA exposure on molecular responses and developmental success in coral larvae

Exposure to polycyclic aromatic carbons (PAHs) poses a growing risk to coral reefs due to increasing shipping and petroleum extraction in tropical waters. Damaging effects of specific PAHs can be further enhanced by the presence of ultraviolet radiation, known as phototoxicity. We tested phototoxic effects of the PAHs anthracene and phenanthrene on larvae of the scleractinian coral Acropora tenuis in the presence and absence of UVA (320–400 nm). Activity of superoxide dismutase (SOD) enzyme was reduced by anthracene while phenanthrene and UVA exposure did not have any effect. Gene expression of MnSod remained constant across all treatments. The genes Catalase, Hsp70 and Hsp90 showed increased expression levels in larvae exposed to anthracene, but not phenanthrene. Gene expression of p53 was upregulated in the presence of UVA, but downregulated when exposed to PAHs. The influence on stress-related biochemical pathways and gene expresson in A. tenuis larvae was considerably greater for anthracene than phenanthrene, and UVA-induced phototoxicity was only evident for anthracene. The combined effects of UVA and PAH exposure on larval survival and metamorphosis paralleled the sub-lethal stress responses, clearly highlighting the interaction of UVA on anthracene toxicity and ultimately the coral’s development.

Assessment of interaction between maternal polycyclic aromatic hydrocarbons exposure and genetic polymorphisms on the risk of congenital heart diseases

The major causes of congenital heart diseases (CHDs) are the interactions of genetic and environmental factors. We conducted a case–control study in 357 mothers of CHDs fetuses and 270 control mothers to investigate the association of maternal PAHs exposure, AHR, CYP1A1, CYP1A2, CYP1B1 and CYP2E polymorphisms, the interaction between PAHs exposure and genetic variants with the risk of CHDs. The higher level PAHs exposure was associated with the risk of CHDs (aOR = 2.029, 95% CI: 1.266, 3.251) or subtypes. The haplotypes of AHR or CYP1A2 were associated with the risk of CHDs: AHR: C-G-A-C: aOR = 0.765; T-A-G-A: aOR = 1.33; CYP1A2: A-T:aOR = 1.75; C-C: aOR = 0.706. When exposed to higher level PAHs, the risk of CHDs among the mothers carrying rs2158041 “C/T or T/T” genotype or rs7811989 “G/A or A/A” genotype in AHR was 1.724 (χ2 = 7.209, P = 0.007) or 1.735 (χ2 = 7.364, P = 0.007) times greater than the aOR in the mothers carrying wild genotype. The multiplicative-scale interactions between PAHs exposure and polymorphisms of CYP1A2 rs4646425 (P = 0.03) or CYP2E1 rs915908 (P = 0.0238) on the risk of CHDs were observed. Our study suggests that maternal AHR polymorphisms may modify the association of PAHs exposure with CHDs, CYP1A2 or CYP2E1 polymorphisms significantly interact with PAHs exposure on CHDs.

Altitudinal and spatial variations of polycyclic aromatic hydrocarbons in Nepal: Implications on source apportionment and risk assessment

Although several global/regional studies have detailed the high level of polycyclic aromatic hydrocarbons in urban areas worldwide, unfortunately, Nepal has never been part of any global/regional regular monitoring plan. Despite few sporadic studies exist, the systematic monitoring and integrated concentration of PAHs in urban region of Nepal are lacking. In this study, the concentrations, sources, and health risk assessment of 16 PAHs in air (n = 34) were investigated in suspected source areas/more densely populated regions of Nepal. Four potential source areas in Nepal were focused as it was conjectured that urban centers in plain areas (Birgunj and Biratnagar) would possibly be more influenced by PAHs as a result of intense biomass/crop residue burning than those in hilly areas (Kathmandu and Pokhara). The overall concentrations of ∑16PAHs ranged from 4.3 to 131 ng/m3 (median 33.3 ng/m3). ∑16PAH concentrations in plain areas were two folds higher than those in hilly areas. PHE was the most abundant followed by FLUA, PYR, and NAP, which accounted for 36%, 15%, 12%, and 9% of ∑16PAHs, respectively. Principal component analysis confirmed that PAHs in highly urbanized areas (Kathmandu and Pokhara) were related to diesel exhausts and coal combustion, while PAHs in less urbanized regions (Birgunj and Biratnagar) originated from biomass and domestic wood combustions. Furthermore, in the urban areas of Nepal, vehicular emission could also influence atmospheric PAHs. The lifetime cancer risk per million populations due to PAH exposures was estimated to be higher for plain areas than that for hilly areas, suggesting a relatively greater risk of cancer in people living in plain areas.

PAHs exposure and occupational health risk assessment of workers in coal tar pitch factory

Objective: To Investigation of industrial sites involving coal tar pitch to detect PAHs in the occupational environment and to assess their occupational health risks to workers. Methods: Taking coal tar pitch enterprises as the research object, and making the occupational health field investigation and inspection. Detecting the 16 PAHs in the samples by high performance liquid chromatography (HPLC) , analyze the PAHs exposed dose of the workers in the place, and using cumulative toxic equivalent quantity method, loss of life expectancy method and carcinogenic risk factor method to assessment worker's occupational health risk. Results: In the 15 posts involved, Some workers' exposed to the total concentration of PAHs is higher than others, the maximum exposure concentration is 1931.45ng/m3. There are different hazard risk levels in different working post due to different processes.The lifetime risk of workers is significantly higher than the acceptable range. Some workers has higher carcinogenic risk and workers' life expectancy loss is up to 1033.95 hours. Conclusion: Part of the coal tar pitch workers exposed to higher concentrations of PAHs, and beyond the occupational exposure limits.And there is a high occupational health risk due to high exposure to PAHs.

Genome-Wide Analysis of mRNA Expression Profiling Identified Lung Cancer-Related Gene in Xuanwei, China.

The morbidity and mortality of lung cancer in Xuanwei (LCXW) is among the highest in China for both males and females and increases constantly. The underlying molecular changes associated with LCXW are still unclear. The purpose of this study was to screen out potential cancer-related genes which may become promising biomarkers of LCXW. Differentially expressed genes (DEGs) were detected by the expression microarrays in 29 paired LCXW tissues (tumor tissue and matched adjacent non-cancerous lung tissues). Integrated with bioinformatic analyses, a literature review was applied for screening out important cancer-related genes. An additional 44 paired LCXW samples were collected to verify the transcription and expression levels of the candidate gene by qRT-PCR and Western blotting. The relationship between the candidate genes and clinical pathological features were evaluated using Fisher's test. mRNA expression microarrays revealed that the LCXW patients harbored 2,424 differentially expressed genes (fold change ≥ 2.0). Of these genes, 1,636 were up-regulated while the other 788 genes were down-regulated. Forty previously reported DNA repair genes associated with PAHs exposure were identified by microarrays. Bioinformatic analyses indicated down-regulated ANXA3 in LCXW patients which was closely related to pathological stage and involved in the regulation of a variety of biological responses. Review of the literature on ANXA3 found its down-regulation was a distinct expression pattern compared with lung cancer occurring in other geographic areas. qRT-PCR and Western blotting confirmed the down-regulation of ANXA3 was associated with LCXW. The correlation analysis of clinical features showed down-regulated ANXA3 was correlated to the progression of pathological stage. The LCXW patients harbored more DEGs, and these DEGs were involved in a wide range of pathways and biological function damage. We preliminarily suggested ANXA3 may be a potential LCXW related gene. ANXA3 may serve as a promising biomarker for diagnosis of LCXW.