Environmental Polycyclic Aromatic Hydrocarbons Exposure Research Articles

Possible relationship between respiratory diseases and urinary concentrations of polycyclic aromatic hydrocarbon metabolites - a pilot study.

This study investigates the potential relationship between exposure to polycyclic aromatic hydrocarbons (PAHs), specifically monohydroxylated metabolites (OH-PAHs), in urine, and the prevalence of respiratory diseases in 2-year-old children residing in two locations within the Czech Republic - České Budějovice (control location) and the historically contaminated mining district of Most. Despite current air quality and lifestyle similarities between the two cities, our research aims to uncover potential long-term health effects, building upon previous data indicating distinctive patterns in the Most population. A total of 248 urine samples were analysed for the presence of 11 OH-PAHs. Employing liquid-liquid extraction with ethyl acetate and clean-up through dispersive solid-phase extraction, instrumental analysis was conducted using ultra-high performance liquid chromatography coupled with tandem mass spectrometry. The incidence of respiratory diseases was assessed through questionnaires administered by paediatricians. The concentrations of OH-PAHs were elevated in urine samples from 2-year-olds in Most compared to those from České Budějovice. The incidence of respiratory diseases showed statistically significant higher levels of OH-PAHs in children from Most, together with a higher incidence of influenza. This association underlines the impact of environmental PAH exposure on children's respiratory health. It suggests that elevated urinary OH-PAH levels indicate an increased risk of developing respiratory diseases in the affected population. Further studies are needed to clarify the possible long-term health effects and to contribute to sound public health strategies.

Environmental and dietary exposure to 24 polycyclic aromatic hydrocarbons in a typical Chinese coking plant

Polycyclic aromatic hydrocarbons (PAHs), known for their health risks, are prevalent in the environment, with the coking industry being a major source of their emissions. To bridge the knowledge gap concerning the relationship between environmental and dietary PAH exposure, we explore this complex interplay by investigating the dietary exposure characteristics of 24 PAHs within a typical Chinese coking plant and their association with environmental pollution. Our research revealed Nap and Fle as primary dietary contaminants, emphasizing the significant influence of soil and atmospheric pollution on PAH exposure. We subjected our data to non-metric multidimensional scaling (NMDS), Spearman correlation analysis, Lasso regression, and Weighted Quantile Sum (WQS) regression to delve into this multifaceted phenomenon. NMDS reveals that dietary PAH exposure, especially within the high molecular weight (HMW) group, is common both within and around the coking plant. This suggests that meals prepared within the plant may be contaminated, posing health risks to coking plant workers. Furthermore, our assessment of dietary exposure risk highlights Nap and Fle as the primary dietary contaminants, with BaP and DahA raising concerns due to their higher carcinogenic potential. Our findings indicate that dietary exposure often exceeds acceptable limits, particularly for coking plant workers. Correlation analyses uncover the dominant roles of soil and atmospheric pollution in shaping dietary PAH exposure. Soil contamination significantly impacts specific PAHs, while atmospheric pollution contributes to others. Additionally, WQS regression emphasizes the substantial influence of soil and drinking water on dietary PAHs. In summary, our study sheds light on the dietary exposure characteristics of PAHs in a typical Chinese coking plant and their intricate interplay with environmental factors. These findings underscore the need for comprehensive strategies to mitigate PAH exposure so as to safeguard both human health and the environment in affected regions.

Delayed clearance of the pro-carcinogen benzo[a]pyrene in PLHC-1 cells when co-exposed to the antifungal drug clotrimazole and effects on the CYP1A biomarker

Cytochrome P450 1 A (CYP1A) is a key enzyme in the metabolism of the polycyclic aromatic hydrocarbon (PAH) benzo[a]pyrene (BaP) in animals, and a biomarker for environmental PAH exposure. The common antimycotic imidazole drug clotrimazole (CLO) has been detected in the aquatic environment and likely co-exists with BaP. Like BaP, CLO can bind to CYP1A enzymes and can act as a CYP1A inhibitor. Co-exposure of BaP with CLO significantly delayed BaP elimination in a fish liver cell line (PLHC-1). Intracellular BaP concentration was 2.4 times higher after 6 h in co-exposed cells, compared to cells exposed to BaP alone. Higher BaP concentrations in cells co-exposed to CLO positively correlated with CLO dose, indicating CLO-mediated delays in BaP clearance. After 24 h, BaP was undetectable irrespective of CLO co-exposure. In contrast, intracellular CLO concentrations remained constant over the 72 h experimental period. Co-exposure of BaP with CLO caused synergistic and time-dependent increases on the CYP1A biomarker both on CYP1A mRNA levels and on CYP1A enzyme activity, in accordance with an apparent delayed BaP elimination in the presence of CLO. These results indicate a toxicokinetic interaction between BaP and CLO on the CYP1A enzyme that delays metabolic clearance of BaP.

Systemic inflammation mediates environmental polycyclic aromatic hydrocarbons to increase chronic obstructive pulmonary disease risk in United States adults: a cross-sectional NHANES study.

This study explored the relationship between environmental polycyclic aromatic hydrocarbons (PAHs) and Chronic obstructive pulmonary disease (COPD), and identified systemic inflammation as a mediator of the increased risk of COPD from PAHs. Data were obtained from 60,936 middle-aged and older Americans recruited in the National Health and Nutrition Examination Survey 2005-2016. Environmental PAHs were measured in terms of urinary concentrations of PAHs metabolites (NAP: 1-hydroxynaphthalene, FLU: 2-hydroxyfluorene, PA: 1-hydroxyphenanthrene, and PYR: 1-hydroxypyrene). We used multifactor logical analysis to figure out the link between PAHs and COPD, and the non-linear relationship was examined using Restricted cubic spline. Spearman correlation analysis was utilized to analyze the connection between PAHs and systemic immune-inflammation index (SII). The results showed that the COPD population had higher NAP (3.550 vs. 3.282, p < 0.001), FLU (2.501 vs. 2.307, p < 0.001), PA (2.155 vs. 2.082, p = 0.005), and PYR (2.013 vs. 1.959, p = 0.008) levels than non-COPD population. In unadjusted logistics analysis, the risk of COPD with log NAP was higher [OR = 1.461, 95% CI (1.258-1.698), p < 0.001]. Upon taking into account, confounders like sex, age, race, and log NAP still increased a possible COPD risk [OR = 1.429, 95% CI (1.224-1.669), p < 0.001]. Similarly, FLU, PA, and PYR significantly increased the risk of COPD (all OR > 1, p < 0.05), both unadjusted and adjusted. Furthermore, Restricted cubic spline demonstrated a strong link between PAHs levels and COPD risk (p < 0.05). Additionally, a Spearman correlation analysis revealed a favorable association between log FLU and log SII (R = 0.43, p = 0.006), while NAP, PA, and PYR levels were not associated with log SII (all p > 0.05). Ultimately, the mediating effect analysis revealed a mediating effect capacity of 5.34% for the SII-mediated association between FLU and COPD. The findings suggest that the risk of COPD is significantly increased when environmental PAHs exposure is at high levels, and that systemic inflammation may be involved in the process.

Association of environmental polycyclic aromatic hydrocarbons exposure with periodontitis in NHANES 2009-2014: A mixtures approach.

Polycyclic aromatic hydrocarbons (PAHs) can invade and cause harm to the human body through various pathways, but there is currently little research on the relationship between mixed-PAHs exposure and periodontitis. The purpose of this study was to examine the effects of mixed-urinary PAHs exposure on periodontitis in adults in the United States. The cross-sectional study included 2749 subjects selected from the National Health and Nutrition Examination Survey (NHANES) 2009-2014 cycles. A professional examination of the periodontal status was conducted to distinguish between periodontitis and non-periodontitis based on the Centers for Disease Control and Prevention/American Academy of Periodontology (CDC/AAP) case definition. Laboratory testing of urine samples was performed to obtain the levels of urinary PAHs. Pearson correlation coefficients were utilized to determine the degree of correlation between urinary PAHs, while weighted binary logistic regression and Bayesian kernel machine regression (BKMR) were employed to evaluate the relationship between urinary PAHs and periodontitis. In a single-exposure model, 3-hydroxyfluorene (OH-3F), 2-hydroxyfluorene (OH-2F), 1-hydroxyphenanthrene (OH-1Ph), and 2-hydroxyphenanthrene and 3-hydroxyphenanthrene (OH-2,3Ph) were positively associated with periodontitis risk. In the mixed-exposure model, BKMR analysis demonstrated that mixed exposure to urinary PAHs was positively associated with periodontitis, with OH-2F being the most critical factor for the overall mixed effects (posterior inclusion probability [PIP]=0.98). Univariate exposure-response function and univariate effects analysis revealed a positive correlation between urinary OH-2F levels and periodontitis. The study reveals a significant positive correlation between exposure to mixed PAHs and periodontitis, with a particular emphasis on the pivotal role of OH-2F. Mitigating PAHs in the environment may serve as a preventive measure against periodontitis and alleviate its global public health burden.

Environmental polycyclic aromatic hydrocarbon exposure is associated with low back pain.

Several studies have assessed the influence of several often-ignored environmental factors on low back pain (LBP), but the effects of environmental polycyclic aromatic hydrocarbon (PAH) exposure on LBP are unclear. During the 2001-2004 cycle of the National Health and Nutrition Examination Survey (NHANES), our study was given to a representative sample of US participants older than 20 (N = 2743). Environmental PAH exposure was calculated using urinary PAH metabolite concentrations.Weighted logistic regression was performed to assess the connection between PAH levels and LBP, with mediation analysis utilised to explore the underlying mechanism.Levels of 1-hydroxynaphthalene (1-OHNa), 2-hydroxynaphthalene (2-OHNa) and total PAHs had a statistically significant positive association with LBP. The odds ratios per 1-unit increase for log-transformed levels of urinary 1-OHNa, 2-OHNa, and total PAHs with LBP were 1.01 (95% CI 1.02-1.19), 1.19 (95% CI 1.04-1.36) and 1.16 (95% CI 1.03-1.32), respectively. The resultsrevealed a strong dose-response association between1-OHNa, 2-OHNa, total PAHs, andLBP risk. Subgroup analysis indicated that 2&3-OHPh may increase the risk of LBP in the lower family income subgroup. Gamma-glutamyl transaminase (GGT), known as a biomarker of oxidative stress, was strongly related to PAHs. The relationship between total PAHs and LBP was mediated in part by GGT. Our study demonstrates associations between environmental PAH exposure and LBP that need more research to determine the precise effects of various PAH compounds on LBP.

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.

Environmental polycyclic aromatic hydrocarbon exposure in relation to metabolic syndrome in US adults

The present study examined the associations of polycyclic aromatic hydrocarbon (PAH) exposure with metabolic syndrome (MetS) and its components. Data were from 5181 US adults recruited in the National Health and Nutrition Examine Survey 2001–2012. Environmental PAH exposure was estimated as concentrations of urinary PAH metabolites. Weighted quantile sum (WQS) regression and modified Poisson regression were separately conducted to estimate the associations of mixed and single PAH metabolites with MetS and its components. WQS regression analyses showed that participants with higher mixed PAH exposure had increased prevalence of MetS (prevalence ratio, 1.12; 95 % confidence interval, 1.06, 1.19), elevated waist circumference (1.07; 1.02, 1.12), elevated fasting blood glucose (1.07; 1.00, 1.14), elevated triglycerides (1.19; 1.09, 1.30), and reduced high-density lipoprotein cholesterol (1.11; 1.03, 1.20). In the models for single PAH metabolites, higher levels of 1-hydroxynaphthalene (1.15; 1.00, 1.32), 2-hydroxynaphthalene (1.20; 1.05, 1.38), 1-hydroxyphenanthrene (1.18; 1.04, 1.34), 2-hydroxyphenanthrene (1.38; 1.22, 1.57), and 1-pyrene (1.19; 1.05, 1.34) were respectively associated with increased prevalence of MetS (highest tertile vs lowest tertile). In addition, linear trends were noted for the associations of these PAH metabolites with MetS (all P for linear association ≤0.047). Smokers, drinkers, and participants with poor diet quality showed stronger associations between certain PAH metabolite with MetS. The findings suggest that the prevalence of MetS and its components increases when PAH exposure is at a high level, and that lifestyle factors, such as cigarette smoking, alcohol consumption, and diet quality, could modify the positive associations of certain PAH exposure with MetS.

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.

Environmental dose of 16 priority-controlled PAHs mixture induce damages of vascular endothelial cells involved in oxidative stress and inflammation

Epidemiological studies have shown that cardiovascular diseases caused by PM2.5 pollution account for the second death rate in China. Polycyclic aromatic hydrocarbons (PAHs) are one important group of persistent organic pollutants absorbed on PM2.5. Though individual PAH is related to vascular disease, the relationship between environmental PAHs exposure and vascular damages is still unclear. To explore the effect of PAHs on blood vessel, human umbilical vein endothelial cells (HUVECs) are treated with 16 priority–controlled PAHs at various concentrations to study their cytotoxicity and morphological alteration. Results showed that, after 48 h treatment, PAHs mixture generally attenuated the ability of wound healing, transwell migration and tube formation of HUVECs (p < 0.01) except for 1 × PAHs in transwell migration. Moreover, PAHs increased the levels of ROS and 8-hydroxy-2′-deoxyguanosine (p < 0.05), indicating that it exceeded the scavenging ability of superoxide dismutase activity. However, PAHs mixture did not increase apoptosis rate, which may be attribute to the difference of PAH concentration and composition between this study and previous reports. Downstream signaling cascades significantly and generally upregulated the relative expression of proteins in Nrf2/HO-1 and NF-ƙB/TNF-α pathway with the activation of oxidative stress, including HO-, TNF-α and Nrf2. In summary, this study suggests that environmental mixture of 16 priority-controlled PAHs can induce the damages of vascular endothelial cells involved in cellular oxidative stress and inflammation.

Low-level exposure to polycyclic aromatic hydrocarbons is associated with reduced lung function among Swedish young adults

BackgroundExposure to polycyclic aromatic hydrocarbons (PAHs) has been linked to adverse pulmonary effects. However, the impact of low-level environmental PAH exposure on lung function in early adulthood remains uncertain. ObjectivesTo evaluate the associations between urinary PAH metabolites and lung function parameters in young adults. MethodsUrinary metabolites of pyrene, phenanthrene, and fluorene were analysed in 1000 young adults from Sweden (age 22–25 years) using LC-MS/MS. Lung function and eosinophilic airway inflammation were measured by spirometry and exhaled nitric oxide fraction (FeNO), respectively. Linear regression analysis was used to evaluate associations between PAH metabolites and the outcomes. ResultsMedian urinary concentrations of 1-OH-pyrene, ∑OH-phenanthrene, and ∑OH-fluorene were 0.066, 0.36, 0.22 μg/L, respectively. We found inverse associations of ∑OH-phenanthrene and ∑OH-fluorene with FEV1 and FVC, as well as between 1-OH-pyrene and FEV1/FVC ratio (adjusted P < 0.05; all participants). An increase of 1% in ∑OH-fluorene was associated with a decrease of 73 mL in FEV1 and 59 mL in FVC. In addition, ∑OH-phenanthrene concentrations were, in a dose-response manner, inversely associated with FEV1 (B from −109 to −48 compared with the lowest quartile of ∑OH-phenanthrene; p trend 0.004) and FVC (B from −159 to −102 compared with lowest quartile; p-trend <0.001). Similar dose-response associations were also observed between ∑OH-fluorene and FEV1 and FVC, as well as between 1-OH-pyrene and FEV1/FVC (p-trend <0.05). There was no association between PAH exposure and FeNO, nor was there an interaction with smoking, sex, or asthma. ConclusionLow-level PAH exposure was, in a dose-response manner, associated with reduced lung function in young adults. Our findings have public health implications due to i) the widespread occurrence of PAHs in the environment and ii) the clinical relevance of lung function in predicting all-cause and cardiovascular disease mortality.

Association between Environmental Polycyclic Aromatic Hydrocarbons Exposure and Insulin Resistance: Using The Second Korean National Environmental Health Survey

Association between Environmental Polycyclic Aromatic Hydrocarbons Exposure and Insulin Resistance: Using The Second Korean National Environmental Health Survey

Polycyclic aromatic hydrocarbon metabolites and mortality risk in an adult population

Occupational polycyclic aromatic hydrocarbons (PAHs) exposure has been shown to increase the risk of various cancers and may be associated with carcinogenic mortality. However, no study has explored the relationship between environmental PAH exposure and mortality in general population. The aim of our study was to explore the association between PAH exposure and all-cause, cardiovascular, and cancer mortality in a general US adult population. We analyzed data from the National Health and Nutrition Examination Survey (NHANES 2001-2006) based on the information in this dataset on 692 males and 717 females. PAH exposure was detected using biomarkers from urine samples. Follow-up data on mortality were derived from initial examination of the subjects until death or 31 December 2006 in the NHANES database. We calculated hazard ratios (HRs) of PAH metabolites among all-cause, cardiovascular, and cancer mortality using the multivariate Cox proportional hazards regression model after adjusting for covariates. Among males, 3-phenanthrene was positively associated with increased risk of all-cause mortality (HR 1.043, 95%CI 1.019-1.066). Female participants with higher 2-napthol (HR 1.043, 95%CI 1.014-1.072), 3-fluorene (HR 2.159, 95%CI 1.233-3.779), and 1-phenanthrene (HR = 1.259, 95%CI 1.070-1.481) levels had increased all-cause mortality. In addition, high 3-phenanthrene (HR 1.333, 95%CI 1.008-1.763) and 1-phenanthrene (HR 1.463, 95%CI 1.126-1.900) levels increased the risk of cardiovascular mortality. However, there were no significant findings for cancer mortality in both genders. Environmental PAH exposure among the adult population is associated with non-carcinogenic but not cancer mortality. Future studies are warranted to determine the underlying mechanisms related to these findings.

Association between polycyclic aromatic hydrocarbons exposure and bone turnover in adults.

Cigarette smoking is a risk factor of osteoporosis and bone fracture. Tobacco smoke contains several polycyclic aromatic hydrocarbons. Thus, we hypothesized that environmental polycyclic aromatic hydrocarbon exposure is associated with bone loss and fracture risk. The present study examined the association between polycyclic aromatic hydrocarbon exposure and bone turnover in the general adult population. A total of 1408 eligible participants from the National Health and Nutrition Examination Survey (NHANES 2001-2006) were included in this cross-sectional analysis. The levels of urinary N-telopeptide and serum bone-specific alkaline phosphatase, which are biomarkers of bone resorption and formation, respectively, were assessed. Meanwhile, polycyclic aromatic hydrocarbon exposure was evaluated using the concentrations of urinary polycyclic aromatic hydrocarbon metabolites. The association between polycyclic aromatic hydrocarbon exposures and N-telopeptide, and bone-specific alkaline phosphatase levels was assessed using a multivariate linear regression model. All polycyclic aromatic hydrocarbon metabolites except 3-phenanthrene were significantly associated with increased N-telopeptide levels (P < 0.05) after adjustment of relevant covariables. However, no significant relationship was observed between polycyclic aromatic hydrocarbon metabolites and bone-specific alkaline phosphatase levels. This relationship remained significant after the participants were assessed according to sex (P < 0.05). Additionally, all polycyclic aromatic hydrocarbon metabolites showed a positive association with N-telopeptide levels in participants aged <60 years (P < 0.05). Polycyclic aromatic hydrocarbon exposure is associated with increased bone resorption among the general adult population in the United States. Further studies must assess the potential mechanisms associated with the adverse effects of polycyclic aromatic hydrocarbon exposure on bone loss.

Polycyclic aromatic hydrocarbon exposure, miRNA genetic variations, and associated leukocyte mitochondrial DNA copy number: A cross-sectional study in China.

Mitochondria DNA was preferentially attacked by the exogenous carcinogens including polycyclic aromatic hydrocarbons (PAHs) relative to nuclear DNA, and nuclear gene variants may account for variability in the mitochondrial DNA copy number (mtDNAcn). However, it remains unclear whether miRNA genetic variations are associated with mitochondrial DNA damage in the PAH-exposed workers. Therefore, we measured the leukocyte mtDNAcn, urinary 1-hydroxypyrene (1-OHPYR), environmental PAH exposure, and miRNA genetic polymorphisms among 544 coke oven workers and 238 healthy control participants. We found that the mtDNAcn in the exposure group (0.60±0.29) was significantly lower than that in the control group (1.03±0.31) (t=18.931, P<0.001). Spearman correlation analysis showed that the peripheral blood leukocyte mtDNAcn had significantly negative correlations with the levels of 1-OHPYR and environmental PAH exposure (P<0.001). Covariance analysis indicated that miR-210 rs11246190 AA, miR-210 rs7395206 CC, and miR-126 rs2297538 GG probably promoted a decrease in leukocyte mtDNAcn in the exposure or control groups (P<0.05). In generalized linear model, miR-210 rs11246190 GG was a protective factor of mtDNAcn, and environmental PAH exposure was the risk factor of the mtDNAcn. In conclusion, the decrease of leukocyte mtDNAcn is the result of a combination of environmental and genetic factors.

Effects of environmental and lifestyle exposures on urinary levels of polycyclic aromatic hydrocarbon metabolites: A cross-sectional study of urban adults in China

Urinary polycyclic aromatic hydrocarbon (PAH) metabolites, biomarkers of internal PAH exposure, are commonly used to explore the effects of PAH on human health. However, the correlation between environmental PAH exposure and the species or levels of urinary PAH metabolites remains unclear. We collected detailed information on PAH exposure sources, including cigarette smoking, cooking, traffic and diet habits via structured questionnaires, and determined 12 urinary monohydroxylated PAH metabolites (OH-PAHs) among 4092 participants from the Wuhan-Zhuhai cohort. Linear mixed models and generalized linear models were conducted to explore the associations of urinary metabolite levels with single or multiple PAH exposure sources. We also calculated the standardized regression coefficients to further compare the contributions of different sources to urinary OH-PAH levels. Our results showed that increasing levels of urinary 1-, 2-hydroxynaphthalene (1-, 2- OHNa) and 2-hydroxyfluorene (2-OHFlu) were significantly correlated with tobacco smoking (all P < 0.01). The concentrations of 1-, 2- OHNa and 9-hydroxyfluorene (9-OHFlu) were positively correlated with dietary intake (all P < 0.05). Individuals who spent a long time in traffic showed elevated levels of 9-OHFlu and 1-hydroxyphenanthrene (1-OHPh) compared with individuals who spent a short time in traffic (all P < 0.05). Self-cooking was associated only with elevated 1-hydroxypyrene (1-OHP) levels. Moreover, good kitchen ventilation resulted in significantly decreased urinary low-molecular-weight OH-PAH levels. These findings suggested that cigarette smoking, self-cooking, high dietary PAH intake and a long time spent in traffic were associated with increased levels of specific urinary PAH metabolites, and good kitchen ventilation effectively reduced the exposure to low-molecular-weight PAHs in self-cooking participants.

Environmental PAH exposure and male idiopathic infertility: a review on early life exposures and adult diagnosis.

The male reproductive system is acutely and uniquely sensitive to a variety of toxicities, including those induced by environmental pollutants throughout the lifespan. Early life hormonal and morphological development results in several especially sensitive critical windows of toxicity risk associated with lifelong decreased reproductive health and fitness. Male factor infertility can account for over 40% of infertility in couples seeking treatment, and 44% of infertile men are diagnosed with idiopathic male infertility. Human environmental exposures are poorly understood due to limited available data. The latency between maternal and in utero exposure and a diagnosis in adulthood complicates the correlation between environmental exposures and infertility. The results from this review include recommendations for more and region specific monitoring of polycyclic aromatic hydrocarbon (PAH) exposure, longitudinal and clinical cohort considerations of exposure normalization, gene-environment interactions, in utero exposure studies, and controlled mechanistic animal experiments. Additionally, it is recommended that detailed semen analysis and male fertility data be included as endpoints in environmental exposure cohort studies due to the sensitivity of the male reproductive system to environmental pollutants, including PAHs.

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

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

Sex-dependent and body weight-dependent associations between environmental PAHs exposure and insulin resistance: Korean urban elderly panel

BackgroundThe prevalence of metabolic diseases rises rapidly with an ageing population. Recent studies suggest the potential involvement of environmental chemicals in insulin resistance (IR) that plays a core role in...

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

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