High Polycyclic Aromatic Hydrocarbons Exposure Research Articles

Using Four Machine Learning Methods to Analyze the Association Between Polycyclic Aromatic Hydrocarbons and Visual Impairment in American Adults: Evidence from NHANES.

The causes of visual impairment are complex and may be influenced by exposure to environmental pollutants. Using data from the 2003-2004 National Health and Nutrition Examination Survey (NHANES), we examined the association between exposure to ten polycyclic aromatic hydrocarbons (PAHs) and vision problems in 1149 U.S. adults. We employed various supervised learning methods, including variable selection techniques such as Lasso and elastic net, weighted quantile sum regression (WQS), and Bayesian kernel machine regression (BKMR), to assess the association between PAHs and the occurrence of visual impairments. The mediation effects between urinary 2-fluorene and inflammation were evaluated using mediation analysis. Both the lasso and elastic net models consistently identified two specific PAH congeners, 2-fluorene and 1-phenanthrene, as significant predictors. The WQS regression revealed a positive relationship between the PAH mixture and visual impairment, with notable contributions from urinary 2-fluorene (weight = 0.39) and 9-fluorene (weight = 0.21). BKMR analysis indicated that the likelihood of visual impairment increases with higher PAH exposure, showing a general upward trend. This trend also revealed a positive association between visual impairment and exposure to four specific PAH metabolites, including 2-fluorene. A significant mediation effect was observed for alkaline phosphatase (p = 0.03), with a proportion mediated of 10.48%. Our findings suggest a significant association between PAHs and visual impairment, with multiple statistical models consistently emphasizing the crucial role of 2-fluorene exposure. This study highlights the importance of considering environmental pollutants as significant contributors to visual health outcomes, providing insights for preventing visual impairment.

Spatiotemporal distributions and ecological risk of polycyclic aromatic hydrocarbons in the surface seawater of Laizhou Bay, China.

The spatial-temporal distribution, source, and potential ecological risk of polycyclic aromatic hydrocarbons (PAHs) in surface seawater from Laizhou Bay were investigated. The total PAH (ΣPAH) concentrations ranged from 277 to 4393 ng/L with an average of 1178 ng/L, thereby suggesting a relatively moderate to high PAH exposure level in Laizhou Bay in comparison to other bays in the world. The composition patterns and source apportionment results revealed that the coal, biomass burning, diesel emissions, and petroleum combustion as well as the combination of these processes were the dominant sources of PAHs in the surface water, which were closely associated with sail process and sewage effluents. The ecological risk assessment indicated that benzo(a)pyrene (BaP), phenanthrene (Phe), luoranthene (Flua), and naphthalene (Nap) would exist ecological risks in most of surface seawater sites, but the probabilistic risk assessment (PRA) results showed that the current level of risk is not as severe as the risk quotient (RQ) results revealed.

The effect of high polycyclic aromatic hydrocarbon exposure on biological aging indicators

BackgroundAging represents a serious health and socioeconomic concern for our society. However, not all people age in the same way and air pollution has been shown to largely impact this process. We explored whether polycyclic aromatic hydrocarbons (PAHs), excellent fossil and wood burning tracers, accelerate biological aging detected by lymphocytes DNA methylation age (DNAmAge) and telomere length (TL), early nuclear DNA (nDNA) hallmarks of non-mitotic and mitotic cellular aging, and mitochondrial DNA copy number (mtDNAcn).MethodsThe study population consisted of 49 male noncurrent-smoking coke-oven workers and 44 matched controls. Occupational and environmental sources of PAH exposures were evaluated by structured questionnaire and internal dose (urinary 1-pyrenol). We estimated Occup_PAHs, the product of 1-pyrenol and years of employment as coke-oven workers, and Environ_PAHs, from multiple items (diet, indoor and outdoor). Biological aging was determined by DNAmAge, via pyrosequencing, and by TL and mtDNAcn, via quantitative polymerase chain reaction. Genomic instability markers in lymphocytes as target dose [anti-benzo[a]pyrene diolepoxide (anti-BPDE)–DNA adduct], genetic instability (micronuclei), gene-specific (p53, IL6 and HIC1) and global (Alu and LINE-1 repeats) DNA methylation, and genetic polymorphisms (GSTM1) were also evaluated in the latent variable nDNA_changes. Structural equation modelling (SEM) analysis evaluated these multifaceted relationships.ResultsIn univariate analysis, biological aging was higher in coke-oven workers than controls as detected by higher percentage of subjects with biological age older than chronological age (AgeAcc ≥ 0, p = 0.007) and TL (p = 0.038), mtDNAcn was instead similar. Genomic instability, i.e., genotoxic and epigenetic alterations (LINE-1, p53 and Alu) and latent variable nDNA_changes were higher in workers (p < 0.001). In SEM analysis, DNAmAge and TL were positively correlated with Occup_PAHs (p < 0.0001). Instead, mtDNAcn is positively correlated with the latent variable nDNA_changes (p < 0.0001) which is in turn triggered by Occup_PAHs and Environ_PAHs.ConclusionsOccupational PAHs exposure influences DNAmAge and TL, suggesting that PAHs target both non-mitotic and mitotic mechanisms and made coke-oven workers biologically older. Also, differences in mtDNAcn, which is modified through nDNA alterations, triggered by environmental and occupational PAH exposure, suggested a nuclear-mitochondrial core-axis of aging. By decreasing this risky gerontogenic exposure, biological aging and the consequent age-related diseases could be prevented.

Urinary polycyclic aromatic hydrocarbon metabolites were associated with hypertension in US adults: data from NHANES 2009-2016.

Polycyclic aromatic hydrocarbons (PAHs) are widely existing organic pollutants in the environment, and their persistence in the environment makes us have to pay continuous attention to their health effects. However, since the American Heart Association updated its definition of hypertension in 2017, few studies have explored the relationship. This study aimed to investigate the relationship between PAH exposure and hypertension after the updated definition of hypertension and explore whether body mass index (BMI) moderates this relationship. A total of 6332 adult participants from the 2009-2016 National Health and Nutrition Examination Survey (NHANES) were examined. Multiple logistic regression and restricted cubic splines were used to analyze the association between urinary polycyclic aromatic hydrocarbon metabolites and hypertension, and the dose-response relationship. Weighted quantile sum (WQS) regression was applied to blood pressure to reveal multiple exposure effects and the relative weights of each PAH. The prevalence of hypertension in the study population was 48.52%. There was a positive dose-response relationship between high exposure to 1-hydroxynaphthalene, 2&3-hydroxyphenanthrene, and the risk of hypertension. Naphthalene metabolites accounted for the most significant proportion of systolic blood pressure, and phenanthrene metabolites accounted for the most significant proportion of diastolic blood pressure. Obese individuals with high PAH exposure were at greater risk for hypertension than individuals with low PAH exposure and normal BMI. Higher prevalence rate and stronger association of metabolites with outcomes were obtained in the general population of the USA under the new guideline. High levels of exposure to PAHs were positively associated with the risk of hypertension, and these effects were modified by BMI.

The effect of maternal polycyclic aromatic hydrocarbons exposure and methylation levels of congenital heart diseases-candidate genes on the risk of congenital heart diseases.

To evaluate the impact of maternal exposure to polycyclic aromatic hydrocarbons (PAHs) and methylation levels of CHDs-candidate genes on the risk of congenital heart diseases (CHDs), and the effect of PAHs exposure on DNA methylation states. A case-control study involving 60 mother -fetus pairs was performed by measuring 1-OHPG concentration in maternal urine and methylation levels of 20 CHDs-candidate genes in cord bloods. Logistic regression models were applied to determine the effect of maternal PAHs exposure and fetal methylation levels on the risk of CHDs. Spearman correlation was performed to correlate PAHs exposure and methylation levels. Maternal higher PAHs exposure was associated with the risk of CHDs (aOR=3.245, 95% CI: 1.060, 9.937) or some subtypes. The methylation levels of 23 amplicons within 11 genes exhibited significant differences between CHDs and controls. Higher methylation of NKX2-5_M1 was associated with decreased risk of CHDs (aOR=0.182, 95% CI:0.034, 0.983). No significant correlations were found between 1-OHPG concentration and methylation levels of NKX2-5_M1. Maternal PAHs exposure was linked with CHDs. Higher methylation of the upstream sequence of NKX2-5 promoter decreased the risk of CHDs. There was no correlation between maternal PAHs exposure and the methylation level of NKX2-5.

Effects of Environmental Polycyclic Aromatic Hydrocarbons Exposure and Pro-Inflammatory Activity on Type 2 Diabetes Mellitus in US Adults.

Polycyclic aromatic hydrocarbons (PAHs) are formed due to natural and anthropogenic activities and known for their potential impact and persistence in the environment. PAHs exposure has been linked to cause adverse health effect including lung cancer, heart conditions and genetic mutations. The understanding of metabolic effects of PAHs exposure is less clear especially in the presence of pro-inflammatory stress like alcoholism or diabetes. The aim of this article is to understand the metabolic effects of PAHs exposure on Type 2 Diabetes Mellitus (T2DM) by analyzing the clinical biomarkers data retrieved from the National Health and Nutrition Examination Survey, Center for Disease Control (CDC NHANES) (2015–16). This study has also accessed the interactive impact of PAHs and other proinflammatory factors, like alcohol intake on the metabolic syndrome on T2DM. We investigated urinary levels of hydroxylated PAHs metabolites (OH-PAHs) along with demographic, clinical and laboratory data. Generalize linear model Univariate factorial ANOVA was used to evaluate the group differences in the demographics, PAH exposure, drinking patterns, clinical data, and biomarker levels. Linear regression model was used to analyze the association of biomarkers, PAH exposure and drinking data. Multivariable regression model was used for multi-independent model to assess comorbidity association and their effect sizes on the clinical outcomes. The results indicated that BMI (p = 0.002), and age (≤0.001) are independent demographic risk factors for T2DM in high PAHs exposure. Acute proinflammatory activity characterized by CRP, is augmented by elevated monocyte levels (p ≤ 0.001) and stepwise addition of 1-Hydroxynapthelene (p = 0.005), and 2-Hydroxynapthelene (p = 0.001) independently. Prevalence of highest average drinks over time is observed in the high PAHs exposure; with males drinking almost twice compared to females in highly exposed population. Pathway response of T2DM shows sexual dimorphism; with males showing association with triglycerides (p ≤ 0.001), and females with CRP (p = 0.015) independently with HbA1C. The arrangement of CRP, absolute monocyte levels, serum triglycerides and average drinks over time predict the HbA1C levels (adjusted R2 = 0.226, p ≤ 0.001) in individuals with high PAHs exposure. Findings from this investigation support the pathological role of high exposure of PAHs in the exacerbation of metabolic disorder syndrome involving T2DM. Sexual dimorphism is reflected in alcohol drinking, with males drinking more in the high PAHs exposure group. Alcohol drinking as an independent factor was associated with the T2DM indicator, HbA1C in individuals with high PAHs exposure.

Effects of polycyclic aromatic hydrocarbons exposure on prognosis of high risk human papillomavirus infection: a prospective cohort study

Objective: To investigate the effects of polycyclic aromatic hydrocarbons (PAHs) exposure on the prognosis of high risk human papillomavirus (HR-HPV) infection. Methods: In this prospective study, 564 patients with low-grade cervical intraepithelial neoplasia confirmed by pathology were selected from the natural cohort population established by our research group in Shanxi province in 2014. Based on the baseline data of demographic characteristics and factors related to HPV infection, the concentrations of 1-hydroxypyrene in urine samples of the patients were determined by high performance liquid chromatography to define the exposure level of PAHs. At baseline survey and follow-up after 24 months, flow-through hybridization was used to detect HPV infection types, and to evaluate the prognosis of HR-HPV (persistent infection, negative conversion, positive conversion and persistent negative status). Results: Of the 564 subjects, 483 completed the follow-up, with a follow-up rate of 85.6% (483/564). Among them, the persistent infection rate was 52.4% (75/143), the persistent homotype infection rate was 35.7% (51/143), the negative conversion rate was 47.6% (68/143), the positive conversion rate was 19.7% (67/340), and the persistent negative rate was 80.3% (273/340). The follow-up results showed that the persistent infection rate (aRR=3.22, 95%CI: 1.85-5.62) and positive conversion rate (aRR=2.84, 95%CI: 1.64-4.94) of HR-HPV in high PAHs exposure group were higher than those in low PAHs exposure group, while the persistent negative rate (aRR=0.55, 95% CI: 0.43-0.70) of HR-HPV in high PAHs exposure group were lower than those in low PAHs exposure group. Based on restrictive cubic spline analysis, the results showed that the effects of PAHs exposure on persistent HR-HPV infection and persistent homotype infection showed an ascending linear dose-response relationship, while on HR-HPV positive conversion and persistent negative status showed an ascending and declining nonlinear dose-response relationship respectively (P<0.01). Conclusions: High PAHs exposure could promote persistent HR-HPV infection and persistent homotypic infection. Reducing PAHs exposure might conducive to HR-HPV continuous negative maintenance. Active prevention and control of PAHs exposure is of great significance to prevent HR-HPV infection and persistent infection.

Analysis of polycyclic aromatic hydrocarbon intake in the US adult population from NHANES 2005–2014 identifies vulnerable subpopulations, suggests interaction between tobacco smoke exposure and sociodemographic factors

Polycyclic aromatic hydrocarbons (PAHs) are a toxic and ubiquitous class of environmental chemicals, products of fuel combustion from human and natural sources. The objective of this study was to identify vulnerable populations for high PAH exposure and variability, to better understand where to target PAH exposure reduction initiatives. Urinary metabolite data were collected from 9517 individuals from the U.S. CDC National Health and Nutrition Examination Survey years 2005–2014 for four parental PAHs naphthalene, fluorene, phenanthrene, and pyrene. We utilized these urinary biomarkers to estimate PAH intake, and regression models were fit for multiple demographic and lifestyle variables, to determine variable effects, interactions, odds of high versus low PAH intake. Smoking and secondhand smoke exposure accounted for the largest PAH intake rate variability (25.62%), and there were strongest interactions between race/ethnicity and smoking or SHS exposure, reflected in a much greater contribution of smoking to PAH intake in non-Hispanic Whites as compared to other races/ethnicities. Increased odds of high PAH intake were seen in older age groups, obese persons, college graduates, midrange incomes, smokers, and those who were SHS exposed. Among the non-smoking population, effects of other demographic factors lessened, suggesting a highly interactive nature. Our results suggest that there are demographic subpopulations with high PAH intake as a result of different smoking behaviors and potentially other exposures. This has human health, environmental justice, and regulatory implications wherein smoking cessation programs, SHS exposure regulations, and public health initiatives could be better targeted towards vulnerable subpopulations to meaningfully reduce PAH exposures.

Impact of Annual Exposure to Polycyclic Aromatic Hydrocarbons on Acute Exacerbation Frequency in Asthmatic Patients.

PurposeExposure to polycyclic aromatic hydrocarbons (PAHs) associated with ambient air particulate matter (PM) poses significant health concerns. Increased acute exacerbation (AE) frequency in asthmatic patients has been associated with ambient PAHs, but which subgroup of patients are particularly susceptible to ambient PAHs is uncertain. We developed a new model to simulate grid-scale PM2.5-PAH levels in order to evaluate whether the severity of asthma as measured by the Global Initiative of Asthma (GINA) levels of treatment is related to cumulative exposure of ambient PAHs.MethodsPatients with asthma residing in the northern Taiwan were reviewed retrospectively from 2014 to 2017. PM2.5 were sampled and analysed for PAHs twice a month over a 72-hour period, in addition to collecting the routinely monitored air pollutant data from an established air quality monitoring network. In combination with correlation analysis and principal component analysis, multivariate linear regression models were performed to simulate hourly grid-scale PM2.5-PAH concentrations (ng/m3). A geographic information system mapping approach with ordinary kriging interpolation method was used to calculate the annual exposure of PAHs (ng/m).ResultsAmong the 387 patients with asthma aged 18 to 93 (median 62), 97 subjects were treated as GINA step 5 (24%). Asthmatics in GINA 5 subgroup with high annual PAHs exposure were likely to have a higher annual frequency of any AE (1 (0–12), p<0.0001). Annual PAHs exposure was correlated with the annual frequency of any exacerbation (r=0.11, p=0.02). This was more significant in the GINA 5 subgroup (r=0.29, p=0.005) and in the GINA 5 subgroup with severe acute exacerbations (r=0.51, p=0.002). Annual PAHs exposure, severe acute exacerbation and GINA steps were independent variables that predict annual frequency of any exacerbation.ConclusionAsthmatic patients in the GINA 5 subgroup with acute exacerbations were more susceptible to the effect of environmental PAHs on their exacerbation frequency. Reducing environmental levels of PAHs will have the greatest impact on the more severe asthma patients.

Filaggrin variations are associated with PAH metabolites in urine and DNA alterations in blood

Dermal chemical exposure is common in many professions. The filaggrin protein is important for the skin barrier and variations in the filaggrin gene (FLG) may influence the uptake of chemicals via the skin, and consequently, the degree of systemic effects. The aim of this study was to investigate, in chimney sweeps with occupational exposure to polycyclic aromatic hydrocarbons (PAH) from soot, the influence of variation in FLG on internal PAH dose and DNA alterations, including epigenetic, previously linked to cancer and cardiovascular disease.We used TaqMan PCR to genotype 151 chimney sweeps and 152 controls for four FLG null variants (R501X, R2447X, S3247X and 2282del4) which cause impaired skin barrier, and FLG copy number variation (12th repeat, CNV12) which potentially is beneficial for the skin barrier. The internal dose of PAH was represented by urinary PAH metabolites (e.g. 1-hydroxypyrene and 3-hydroxybenzo[a]pyrene) that we measured by LC-MS/MS. We measured epigenetic alterations (methylation of AHRR and F2RL3) in blood by pyrosequencing; and DNA alterations (telomere length and mitochondrial DNA copy number) by real-time PCR. Hypomethylation of AHRR or F2RL3 is a risk factor for lung cancer and shorter telomere length a risk factor for cardiovascular disease.The frequencies of FLG null were 8.6 and 11.8% (p = 0.35), and CNV12 27.8 and 19.7% (p = 0.09) in chimney sweeps and controls, respectively. We found that among chimney sweeps working predominately with soot sweeping (high PAH exposure), CNV12 carriers had lower concentrations of PAH metabolites in urine compared with non-carriers (median 1-hydroxypyrene = 0.37 vs 0.86 μg/g creatinine respectively; p = 0.025 by linear regression models adjusted for age, BMI and smoking) compared to sweeps not carrying CNV12. Further, FLG null was associated with approximately 2.5% higher methylation of F2RL3 (cg03636183, p = 0.019 after adjustment for exposure group, age, BMI and smoking). FLG null was associated with approximately 7% shorter telomere length (p = 0.015, adjusted model).Our results suggest that FLG variations may influence the dose of PAH in highly exposed workers, possibly via dermal uptake. It also suggests that FLG variation may influence the degree of (epi)genotoxicity in the body. FLG variation is common in the working population and should be considered in risk assessment.

Risk of congenital heart diseases associated with NAT2 genetic polymorphisms and maternal polycyclic aromatic hydrocarbons exposure

N-Acetyltransferase 2 (NAT2) is a phase II xenobiotic-metabolizing enzyme participating in the detoxification of toxic arylamines and aromatic amines. The present study was designed to investigate whether maternal NAT2 genetic polymorphisms are associated with fetal susceptibility to congenital heart diseases (CHDs) and to assess whether the risk is modified by polycyclic aromatic hydrocarbons (PAHs) exposure. We conducted a hospital-based case-control study to investigate the association of NAT2 gene polymorphisms (rs1799930 G/A, rs1208 A/G, and rs1799931 G/A) and the combinations of PAHs exposure and genetic variants with the risk of CHDs. Three hundred fifty-seven mothers of CHDs fetuses and 270 control mothers were recruited. Logistic regression models for the risk of CHDs were applied to determine the effect of NAT2 polymorphisms, as well as gene-exposure interactions. Our study did not demonstrate an association of maternal NAT2 genetic polymorphisms alone with CHDs occurrence. However, we found that certain genetic polymorphisms of NAT2 in the present of high PAHs exposure have a higher risk of CHDs. Our study suggests that the risk of CHDs associated with maternal NAT2 gene polymorphisms is potentiated by PAHs exposure.

Role of polycyclic aromatic hydrocarbons as a co-factor in human papillomavirus-mediated carcinogenesis

BackgroundHuman papillomavirus (HPV) is an etiological agent of cervical cancer. Yet co-factors are believed to be involved in HPV-mediated carcinogenesis. Polycyclic aromatic hydrocarbons (PAHs) are considered as one of these co-factors. Epidemiologic studies have associated high PAH exposure with increased risk for cancer development. To date, many studies focus on benzo[a]pyrene, however, the role of other PAHs should not be neglected. This study aimed to compare the potential of different PAHs as a co-factor in HPV-mediated carcinogenesis, and to investigate the possible mechanisms involved.MethodsThe effect of 17 PAHs on high-risk HPV (HPV16) were examined in this study. HPV16 E7 oncogene was expressed in primary cells extracted from baby rat kidney and treated with PAHs. The co-transforming ability of PAHs were measured by colony formation index according to the number and size of transformed colonies. Effects of PAHs on proliferation of HPV-null (C33A) and –infected (CaSki) were examined using CCK-8 assay. Wound healing assay and matrigel invasion chambers were used to investigate effects of PAHs on cell motility and invasivion of HPV-null (MCF7, C33A) and –infected (SiHa) cells.ResultsBenzo[a]pyrene (BaP), dibenz[a,h]anthracene (DBA) and indeno[1,2,3-cd]pyrene (IDP) showed the greatest co-transforming potential in the baby rat kidney cell system. Short-term exposure to BaP, DBA, IDP and pyrene (PR) did not affect proliferation of C33A or CaSki cells, however, long-term exposure of these four PAHs led to dramatic increase in growth rate of CaSki cells by 120–140%. Besides, exposure of PAHs has an effect on cell motility and invasiveness of C33A and SiHa cells, but not for MCF7 cells. Exposure of BaP and DBA enhanced migration (1.26 to 1.40-fold) and invasion (1.68 to 1.94-fold) capacity of C33A cells. Intriguingly, exposure of all four types of PAHs boosted the migration (1.12 to 1.28-fold) and invasion (1.26 to 1.40-fold) capacity of SiHa cells.ConclusionsOur results indicate that exposure to PAHs can be a key co-factor in HPV-related cancer development. They could act on all three stages, namely initiation, promotion and progression. Further study is needed to unveil the mechanisms by which PAHs interact with HPV to cause malignancy.

Women’s occupational exposure to polycyclic aromatic hydrocarbons and risk of breast cancer

ObjectiveTo estimate the association between occupational polycyclic aromatic hydrocarbon (PAH) exposure and female breast cancer.MethodsLifetime work histories for 1130 cases and 1169 controls from British Columbia and Ontario (Canada) were...

Heavy Exposure of Waste Collectors to Polycyclic Aromatic Hydrocarbons in a Poor Rural Area of Middle China.

Manual collection and open-air incineration of waste materials is a common practice in rural regions of China and beyond. Low-temperature combustion of rubber and plastic waste generates high levels of airborne polycyclic aromatic hydrocarbons (PAHs). We investigated ten urinary hydroxylated PAH metabolites (OH-PAHs), the oxidative damage biomarker (8-hydroxy-deoxyguanosine, 8-OHdG), and four serum biomarkers including gamma-glutamyl transferase (GGT) and alanine aminotransferase (ALT) in 41 waste collectors and 122 control subjects residing in the same or a distant rural village in Henan Province. The level of PAH metabolites in urine (median: 17.24 μg/g Cre) was twice that of controls living in the same area without an occupational history involving waste collection (median: 8.16 μg/g Cre) and thrice that of controls living 30 km away (median: 6.07 μg/g Cre). The concentrations of OH-PAHs were positively associated with urinary 8-OHdG levels (β = 0.283, p < 0.05). Serum GGT and ALT were slightly increased in waste collectors. Urinary 8-OHdG levels were similar in one-year and longer-term workers, suggesting that rubber and plastic waste collection/incineration carries a high PAH exposure risk. These data provide solid baseline information, emphasizing the importance of monitoring the long-term health outcomes of waste collectors and changes in exposure patterns associated with rural development and regulation of waste disposal.

High Urinary Polycyclic Aromatic Hydrocarbon Concentrations in Bomet County, Kenya, a Region With a High Incidence of Esophageal Squamous Cell Carcinoma

Abstract 43 Background: Polycyclic aromatic hydrocarbons (PAHs) are a group of more than 100 compounds that are formed during incomplete combustion of organic materials, many of which have been classified as known carcinogens. Exposure to PAHs has been suggested as an important risk factor for developing esophageal squamous cell carcinoma (ESCC) in several high-incidence areas, such as China and Iran, but corresponding PAH assessments have not been conducted in East Africa, another ESCC hot spot. To assess the internal uptake of PAH as a result of external exposures, body fluids and tissues can be monitored for PAHs or their metabolites. The primary aim of this study was to quantify the concentration of seven PAH urine metabolites in a cross-section of participants from Bomet, Kenya, an endemic area for ESCC. An additional aim was to assess demographic and lifestyle factors that may be associated with PAH metabolites. Methods: A community-based sample of 294 asymptomatic adults were recruited. Participants collected spot urine specimens and completed a questionnaire. Urine specimens were analyzed at the National Center for Environmental Health at the Centers for Disease Control—the same lab has performed similar analyses on urine samples from the US National Health and Nutrition Examination Survey (NHANES). The seven PAH analytes were hydroxylated metabolites of naphthalene, fluorene, phenanthrene, and pyrene. Median creatinine-adjusted PAH metabolite concentrations (nanogram per gram of creatinine) were compared by all relevant questionnaire items. Results: All seven measured PAH metabolites in the study population were markedly elevated compared with the US population. For example, the median value for 1-hydroxypyrene in Bomet was 1,190 ng/g in males versus 106 ng/g in NHANES, and 2,840 ng/g in females versus 133 ng/g in NHANES. Age (&lt; 50 years), sex (female), and performing indoor cooking were significantly ( P &lt; .01) associated with higher PAH concentrations for all measured metabolites. Regular tobacco use was not reported by many participants (19%) and was not associated with PAH concentrations. Conclusion: PAH metabolite concentrations in Bomet were high compared with the US population. Elevated PAH concentrations were associated with age, sex, and indoor cooking. Additional studies are needed to define the association between high PAH exposure and the risk of developing ESCC as well as to determine the sources of PAH exposure in this high-risk population. Funding: The African Organization for Research and Training in Cancer’s Beginning Investigator Grant for Catalytic Research (BIG Cat) Program, in collaboration with the US National Institutes of Health’s National Cancer Institute, Office of International Affairs. AUTHORS' DISCLOSURES OF POTENTIAL CONFLICTS OF INTEREST No COIs from the authors.

Occupational exposure to polycyclic aromatic hydrocarbons and lymphatic and hematopoietic neoplasms: a systematic review and meta-analysis of cohort studies.

Data on the risk of lymphatic and hematopoietic neoplasms among workers whose jobs entail high exposure to polycyclic aromatic hydrocarbons (PAH) are sparse, and mainly based on small-size studies. We carried out a systematic review of occupational cohort studies that reported results on incidence or mortality from Hodgkin lymphoma (HL), non-Hodgkin lymphoma (NHL), leukemia or multiple myeloma (MM) among workers exposed to PAH. We computed meta-analytic estimates using a random effect model. Meta-relative risk (meta-RR) was computed separately by each type of neoplasm, job or industry. We identified 41 studies (12 in iron and steel foundries, 11 in aluminum plant, 6 in cokeries, 6 in carbon electrode manufacturing, 2 on asphalt workers, 2 on creosote-exposed workers, 1 on tar distillery workers and 1 evaluating both tar distillery workers and roofers). No significant excess risk of any lymphatic and hematopoietic neoplasms was found among workers employed in jobs or industries entailing high PAH exposure. Among 18 meta-analytic estimates by job or industry and type of neoplasm, 16 were close to unit, i.e., between 0.72 and 1.27, whereas the meta-RR was 1.38 [95% confidence interval (CI) 0.95-2.01] for HL in foundry workers and 2.01 (95% CI 0.96-4.22) for NHL in workers exposed to creosote. There was no association between occupation entailing high PAH exposure and risk of MM or leukemia.

Excretion of polycyclic aromatic hydrocarbon metabolites (OH-PAHs) in cattle urine in Ghana

Previous studies of polycyclic aromatic hydrocarbons (PAHs) in particulate matter, soils and livers of wild rats indicated that the city centre of Kumasi, Ghana has been severely polluted with high cancer potency. Cattle urine were therefore collected from Kumasi (urban) and Offinso (rural), Ghana: to determine concentrations of urinary PAH metabolites (OH-PAHs); and find their association with sex; and to estimate exposure of cattle to PAHs from the different sites. From the results, geometric mean concentrations (adjusted by specific gravity), GMSG, showed that 2-OHNaphthalene (2-OHNap) was the most abundant OH-PAH in cattle urine from all study sites, and naphthalene-containing-mothballs might have contributed significantly to the levels. There was no significant difference between urinary OH-PAHs concentrations in cattle from urban and rural sites except for 2-OHPhe and 4-OHPhe, and similar to urban areas, rural sites could also be polluted with PAHs. GMSG of 2-OHNap in cattle urine in Kokote (21.9 ± 6.51 ng/mL; a rural area), was significantly higher compared to the other sites followed by Oforikrom (4.15 ± 4.37 ng/mL; urban). The GMSG concentration (ng/mL) of the sum of OH-PAHs decreased in the order, Kokote (44.7) > Oforikrom (7.87) > Saboa (6.98) > Santasi (6.68) > and Twumasen Estate (5.23). The high concentrations of urinary 2-OHNap, 2-3-OHFlu, 2-OHPhe, 3-OHPhe and 4-OHPhe in Kokote indicated high PAHs exposure to cattle in this area or different/specific source of PAHs exposure. GMSG of 2-OHNap was significantly higher in male cattle compared to females while 1-9-OHPhe was significantly higher in females.

Polycyclic aromatic hydrocarbon exposure, miR-146a rs2910164 polymorphism, and heart rate variability in coke oven workers

BackgroundExposure to ubiquitous polycyclic aromatic hydrocarbons (PAHs) has been associated with decreased heart rate variability (HRV). Evidence accumulates that microRNAs (miRNAs) might be the intermediate factors between environmental exposures and their adverse health effects. Single nucleotide polymorphisms (SNPs) in miRNA genes may affect phenotypes and disease morbidity. ObjectiveWe sought to investigate the influences of four well-studied SNPs in miRNA genes (rs2910164, rs11614913, rs2292832, and rs3746444) on HRV, and their modifying effects on the associations between PAH exposure and HRV. MethodsWe measured the concentrations of ten urinary monohydroxy PAHs (OH-PAHs), seven HRV parameters, and genotypes of these four SNPs in 1222 coke oven workers. ResultsThere were significant differences among different rs2910164 genotype carriers in terms of all seven HRV indices: workers with rs2910164 CC genotype had significant lower HRV than those with GG or GC genotype (P<0.05). The number of rs2910164 C allele was negatively associated with HRV indices in the high PAH exposure group (β<0, P<0.05), and the association between rs2910164 and high-frequency (HF) power was significantly stronger in high exposure group (Pinteraction=0.042). Interestingly, the negative associations between the sum of 10 OH-PAHs and HRV (β<0, P<0.05) were significantly or marginally significantly stronger in workers with rs2910164 CC genotype (Pinteraction≤0.050). ConclusionsCoke oven workers with miR-146a rs2910164 CC genotype may be more susceptible to decreased HRV. The modifying effect of rs2910164 on the PAHs-HRV associations suggested miR-146a may mediate the effects of PAH exposure on HRV.

Repeatedly high polycyclic aromatic hydrocarbon exposure and cockroach sensitization among inner-city children

BackgroundExposures to traffic-related air pollutants including polycyclic aromatic hydrocarbons (PAH) have been associated with the development and exacerbation of asthma. However, there is limited evidence on whether these pollutants are associated with the development of cockroach sensitization, a strong risk factor for urban asthma. We hypothesized that repeatedly high PAH exposure during childhood would be associated with increased risk of new cockroach sensitization. MethodsAs part of the research being conducted by the Columbia Center for Children’s Environmental Health (CCCEH) birth cohort study in New York, a spot urine sample was collected from children at age 5 years (2003–2008) and again at age 9–10 years (2008–2012; n=248) and analyzed for 10 PAH metabolites. Repeatedly high PAH (High–High) exposure was defined as measures above median for age 5 PAH metabolites at both time points. Child blood samples at age 5 and 9 years were analyzed for total, anti-cockroach, mouse, dust mite, cat and dog IgE. Relative risks (RR) were estimated with multivariable modified Poisson regression. ResultsIndividual PAH metabolite levels, except for 1-naphthol (1-OH-NAP), increased by 10-60% from age 5 to age 9–10. The prevalence of cockroach sensitization increased from 17.6% (33/188) at age 5 to 33.0% (62/188) at 9 years (p=0.001). After controlling for potential covariates including cockroach sensitization at age 5 in regression analyses, positive associations were found between repeatedly high exposure (High–High) to 1-OH-NAP, 3-hydroxyphenanthrene (3-OH-PHEN), or 1-hydroxypyrene (1-OH-PYR) and cockroach sensitization at age 9 (p-values<0.05). Compared to Low–Low exposure, the relative risk (RR) [95% CI] with repeatedly high exposure was 1.83 [1.06–3.17] for 1-OH-NAP, 1.54 [1.06–2.23] for 3-OH-PHEN, and 1.59 [1.04–2.43] for 1-OH-PYR. ConclusionsRepeatedly high levels of urinary PAH metabolites during childhood may increase likelihood of sensitization to cockroach allergen in urban inner-city children at age 9 years.

Polycyclic aromatic hydrocarbon (PAH) exposure and oxidative stress for a rural population from the North China Plain.

Polycyclic aromatic hydrocarbons (PAHs) belong to a class of ubiquitous pollutants and are possibly associated with adverse health effects. In this study, we aimed to assess PAH exposure by measuring the hydroxylated metabolites (hydroxy-PAHs) in urine samples of a rural population from the North China Plain and to explore the possible associations between PAH exposure and oxidative stress indicated by urinary malondialdehyde (MDA) and 8-hydroxy-2′-deoxyguanosine (8-OHdG). High levels of urinary hydroxy-PAHs were observed, with the geometric mean concentrations of 0.57, 2.2, 5.0, 7.0, and 16.6 μg g−1 creatinine for 1-hydroxypyrene, hydroxyphenanthrenes, hydroxyfluorenes, hydroxybiphenyls, and hydroxynaphthalenes, respectively. Particularly in the winter season, the exposures were 2.3–6.0-fold of those in the spring. Corresponding to PAH exposure, levels of urinary MDA were positively associated with hydroxy-PAHs after controlling for confounders in the linear regression models (p < 0.05). An estimation indicated 21.3–39.3 % increment of urinary MDA per one-fold increase of hydroxy-PAHs. In contrast, no significant correlation was found between urinary 8-OHdG and hydroxy-PAHs; alternatively, living at the e-waste recycling site was found a significant factor on this oxidative DNA damage. These results provide evidence on high PAH exposure and the induction of oxidative stress on lipid peroxidation for this rural population.