Levels Of Polycyclic Aromatic Hydrocarbons Metabolites Research Articles

Longitudinal joint effects of polycyclic aromatic hydrocarbons exposure and genetic susceptibility on fasting plasma glucose: A prospective cohort study of general Chinese urban adults

The effects of environmental polycyclic aromatic hydrocarbons (PAHs) exposure on glycemic regulation and the underlying genetic mechanism were still unclear. This study aimed to analyze the longitudinal joint effects of PAHs exposure and genetic susceptibility on fasting plasma glucose (FPG) through a longitudinal study. We included 4104 observations (2383 baseline participants and 1721 6-year follow-up participants) from Wuhan-Zhuhai cohort. Ten urinary PAHs metabolites and FPG were measured at both baseline and follow-up. We constructed the polygenic risk scores (PRS) of FPG from the corresponding genome-wide association studies. Linear mixed models were used to explore the associations of urinary PAHs metabolites or FPG-PRS on FPG levels in the repeated-measure analysis. Besides, the longitudinal relationships of urinary PAHs metabolites, FPG-PRS, and their joint effects on FPG change over 6 years were evaluated by linear regression models. Compared with participants with persistent low levels of urinary total PAHs metabolites, hydroxynaphthalene, and hydroxyphenanthrene, participants with persistent high levels had average decreases of 0.173, 0.188, and 0.263 mmol/L for FPG change over 6 years, respectively. Each 1-unit increase of FPG-PRS was associated with a 0.531 mmol/L for FPG change over 6 years. Besides, compared with participants with high FPG-PRS and persistent low levels of urinary total hydroxynaphthalene, hydroxyfluorene, and hydroxyphenanthrene, participants with low FPG-PRS and persistent high levels had average decreases of 0.322, 0.567, and 0.419 mmol/L for FPG change over 6 years. Our findings demonstrated that high-level PAHs exposure was longitudinally associated with an average decrease of FPG over 6 years, and low FPG genetic risk can enhance the above associations. Our findings emphasized the hypoglycemic effect of PAHs exposure, shed new light on the complex effects between PAHs exposure and genetic factors in the prevention of high FPG, and might provide some clues for the development of potential hypoglycemic agents.

Effect of polycyclic aromatic hydrocarbon exposure on amnestic mild cognitive impairment and Alzheimer’s disease: A matched case-control study

There is an emerging body of evidence concerning the neurological effect of air pollutants on cognitive function and increased risk of neurodegeneration. Although previous studies have suggested that polycyclic aromatic hydrocarbons (PAHs) are neurotoxic, the effect of PAHs exposure on neurodegeneration remains unclear. This study aimed to investigate the association between PAH exposure and the risk of developing amnestic mild cognitive impairment (aMCI) and Alzheimer’s disease (AD). For this matched case-control cross-sectional study, we recruited patients aged ≥50 years diagnosed with aMCI and AD from the Samsung Medical Center, Seoul, Korea, between 2014 and 2019. For each patient, we randomly selected four cognitively healthy controls through frequency matching based on sex, age group, and education level. Urinary levels of four PAH metabolites, 1-hydroxypyrene (1-OHP), 1-hydroxyphenanthrene (1-OHPhe), 2-hydroxyfluorene (2-OHFlu), and 2-naphthol (2-NAP), were measured. A conditional logistic regression model was used to evaluate the association, adjusting for potential confounders. A total of 212 patients with aMCI with 848 matched controls, and 267 patients with AD with 1068 matched controls were included in the analyses to estimate the risk of PAH exposure. We found that elevated urinary levels of PAH metabolites (specifically, 1-OHP and 2-NAP) were significantly associated with an increased risk of aMCI and AD. An increase of one unit in log-transformed level of urinary 1-OHP was associated with a 1.15- and 1.16-times higher risk of aMCI and AD, respectively. An increase of one unit in log-transformed level of urinary 2-NAP was associated with a 1.11- and 1.13-times higher risk of aMCI and AD, respectively. These findings indicate that PAH exposure may increase the risk of aMCI and AD, especially for the elderly population. Considering the widespread distribution of PAHs in the environment, reducing PAH exposure may be an effective strategy for the prevention of neurodegenerative diseases.

Seasonal variation in urinary PAH metabolite levels and associations with neonatal birth outcomes.

Previous studies have demonstrated that exposure to polycyclic aromatic hydrocarbons (PAHs) can affect maternal and infant health. However, the conclusions regarding the effects of seasonal PAH exposure on maternal and infant health have been inconsistent. To further elucidate this issue, this study included data from 2282 mother-infant pairs in the Zuni birth cohort. The objective was to investigate the association between maternal late-pregnancy urinary PAH metabolite concentrations and neonatal birth outcomes during the heating and non-heating seasons. The results demonstrated that PAH exposure in Zunyi was primarily dominated by 2-OHNAP and 1-OHNAP and that the concentrations of PAH metabolites were significantly higher during the heating season. Furthermore, PAH metabolite exposure was found to affect neonatal birth weight, birth length, and parity index with seasonal differences. Further dose-effect analyses revealed nonlinear relationships and seasonal differences between PAH metabolites and neonatal birth weight, birth length, and parity index. Bayesian kernel mechanism regression modeling demonstrated that the inverted U-shaped relationship between PAH metabolites and neonatal birth weight and parity index was exclusive to the heating season. Consequently, it can be posited that maternal exposure to PAH metabolites during late pregnancy exerts a detrimental influence on neonatal growth and development, which is further compounded by the use of heating fuels. This highlights the necessity to either control or alter the use of heating fuels during pregnancy.

Urinary polycyclic aromatic hydrocarbon metabolites and hyperlipidemia: NHANES 2007-2016.

The relationships between urinary polycyclic aromatic hydrocarbon (PAH) metabolites and hyperlipidemia have not been thoroughly studied. The primary goal of this research focused on investigating the linkage between PAH metabolite concentrations in urine and hyperlipidemia prevalence within US adults. A cross-sectional analysis was conducted using data from the 2007-2016 National Health and Nutrition Examination Survey (NHANES). Logistic regression models were used to assess correlations between urinary PAH metabolite levels and the risk of hyperlipidemia, while restricted cubic spline models were used to examine dose‒response relationships. Subgroup and interaction analyses were performed to further elucidate these associations. Weighted quantile sum (WQS) regression analyzed the cumulative impact of various urinary PAH metabolites on hyperlipidemia risk. This study included 7,030 participants. Notably, individuals in the highest quintile of urinary PAH metabolite concentrations exhibited a significantly elevated prevalence of hyperlipidemia, even after comprehensive adjustments (odds ratio [OR]: 1.33, 95% confidence interval [CI]: 1.01-1.75). Moreover, elevated levels of 1-hydroxyphenanthrene and 2-hydroxynaphthalene in the fourth quintile and 2-hydroxyfluorene in the third, fourth, and fifth quintiles demonstrated positive correlations with the prevalence of hyperlipidemia. These associations persisted across subgroup analyses. Additionally, a positive correlation between the urinary PAH metabolite mixture and hyperlipidemia (positive model: OR = 1.04, 95% CI: 1.00-1.09) was observed in the WQS model, and 2-hydroxynaphthalene showed the most substantial contribution. The cross-sectional analysis identified a significant correlation between urinary PAH metabolite and hyperlipidemia prevalence within the US demographic, with 2-hydroxynaphthalene being the predominant influencer. These findings underscore the need to mitigate PAH exposure as a preventive measure for hyperlipidemia.

Impact of urinary PAHs on psoriasis risk in U.S. adults: Insights from NHANES.

Exposure to environmental pollutants is increasingly recognized as a risk factor for the development of psoriasis. Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous in the air and might induce reactions such as oxidative stress. Nevertheless, it is still unclear if PAHs have any influence on the prevalence of psoriasis over the entire population of the United States. The objective of this study was to assess the association between urine PAHs and psoriasis. The research included 3,673 individuals aged 20 years or older who participated in the 2003-2006 and 2009-2012 National Health and Nutrition Examination Surveys (NHANES). We employed logistic regression models to evaluate the relationship between levels of urine PAH metabolites and psoriasis and smoothed curve fitting to illustrate the concentration-response relationship. Additionally, subgroup and interaction analyses were conducted to elucidate these associations. Furthermore, we employed weighted quartile sum (WQS) regressions to examine the distinct effects of individual and mixed urine PAH metabolites on psoriasis. However, it is important to note that the NHANES sample may be subject to selectivity and self-reporting bias, which may influence the data' generalisability. We observed that the highest tertiles of 2-NAP and 2-FLU had a 63% (95% CI 1.02, 2.61) and 83% (95% CI 1.14, 2.96) higher odds of association with psoriasis prevalence, respectively. Meanwhile, tertile 2 and tertile 3 of 3-PHE were also significantly associated with psoriasis, with higher odds of 65% (95% CI 1.01, 2.69) and 14% (95% CI 1.17, 3.00), respectively. The subgroup analyses revealed a significant correlation between urine PAH metabolites and the odds of psoriasis in specific groups, including males, aged 40-60 years, with a BMI > 30, and those with hyperlipidemia. In the WQS model, a positive association was found between the combination of urine PAH metabolites and psoriasis (OR 1.43, 95% CI 1.11, 1.84), with 2-FLU being the most prevalent component across all mixtures (0.297). Our findings indicate a significant association between urine PAH metabolites and the odds of psoriasis prevalence in adults. Among these metabolites, 2-FLU demonstrated the most prominent impact. Controlling PAH exposure, as an important strategy for minimizing exposure to environmental contaminants and lowering the risk of psoriasis, is critical for raising public knowledge about environmental health and preserving public health.

Non-carcinogenic and cumulative risk assessment of exposure of kitchen workers in restaurants and local residents in the vicinity of polycyclic aromatic hydrocarbons

Polycyclic aromatic hydrocarbons (PAHs) are often formed when organic substances do not burn completely. This study evaluates the non-carcinogenic and cumulative risks associated with PAHs levels by testing blood and urine samples in kitchen workers and residents near restaurants in Shiraz, Iran. Metabolites of PAH in the urine samples as well as clinical parameters in the blood samples were measured. The non-carcinogenic and cumulative risk assessments from exposure of the study groups to PAH metabolites were also evaluated. The highest average concentrations of PAH metabolites were related to kitchen workers (2126.7 ng/g creatinine (ng/g cr)). The metabolites of 1-Hydroxypyrene (1-OHP) and 9-Phenanthrene (9-OHPhe) had the highest and lowest mean concentrations, respectively. A direct correlation was observed between the levels of PAH metabolites with malondialdehyde (MDA) and total antioxidation capacity (TAC) levels (p < 0.05). Hazard Index (HIi) was obtained less than one (HIi < 1), indicating low-risk negative health impacts on the target groups. Nevertheless, conducting more studies to determine the health status of these people is quite evident.

Exposure to phenols, chlorophenol pesticides, phthalate and PAHs and mortality risk: A prospective study based on 6 rounds of NHANES

ObjectivesHuman exposure to various endocrine disrupting chemicals (EDCs) is widespread and long-lasting. The primary objective of this study was to prospectively evaluate the association of combined exposure of phenols, chlorophenol pesticides, phthalate and polycyclic aromatic hydrocarbons (PAHs) and mortality risk in a representative US population. MethodsThe data on urinary levels of phenols, chlorophenol pesticides, phthalates, and PAH metabolites, were collected from participants aged ≥20 years in six rounds of the National Health and Nutrition Examination Survey (NHANES) (2003–2014). NHANES-linked death records up to December 31, 2015 were used to ascertain mortality status and cause of death. Cox proportional hazards and competing risk models were mainly used for chemical and mortality risk association analysis. The weighted quantile sum (WQS) regression and the least absolute shrinkage and selection operator regression were employed to estimate the association between EDC co-exposure and mortality risk. ResultsHigh levels of mono-n-butyl phthalate, monobenzyl phthalate, and 1-napthol were significantly associated with increased risk of all cause, cardiovascular disease (CVD) and cancer mortality among all participants. WQS index was associated with the risks of all-cause (hazard ratio [HR] = 1.389, 95%CI: 1.155–1.669) and CVD mortality (HR = 1.925, 95%CI: 1.152–3.216). High co-exposure scores were associated with elevated all-cause (HR = 2.842, 95% CI: 1.2.094–3.858), CVD (HR = 1.855, 95% CI: 1.525–2.255), and cancer mortality risks (HR = 2.961, 95% CI: 1.468–5.972). The results of subgroup analysis, competing risk model, and sensitivity analysis were generally consistent with the findings from the main analyses, indicating the robustness of our findings. ConclusionsThis study provided the first epidemiological evidence that co-exposure to EDC at fairly low levels contributed to elevated mortality risk among US adults. The underlying mechanisms for the effects of EDC co-exposure on human health are worthy of future exploration.

Investigating industrial PAH air pollution in relation to population exposure in major countries: A scoring approach

Polycyclic aromatic hydrocarbons (PAHs) are common air pollutants worldwide, associated with industrial processes. In the general population, both modeling and field studies revealed a positive correlation between air PAH concentrations and urinary PAH metabolite levels. Many countries lack population urinary data that correspond to local PAH air concentrations. Thus, we proposed a scoring-based approximate approach to investigating that correlation in selected countries, hypothesizing that PAH air concentrations in selected regions could represent the national air quality influenced by industrial emission and further correlate to PAH internal exposure in the general population. This research compiled 85 peer-reviewed journal articles and 9 official monitoring datasets/reports covering 34 countries, 16 of which with both atmospheric PAH data and human biomonitoring data. For the air pollution score (AirS), Egypt had the highest AirS at 0.94 and Pakistan was at the bottom of the score ranking at −1.95, as well as the median in the UK (AirS: 0.50). For the population exposure score (ExpS), China gained the top ExpS at 0.44 and Spain was with the lowest ExpS of −1.52, with the median value in Italy (ExpS: 0.43). Through the correlation analysis, atmospheric PAHs and their corresponding urinary metabolites provided a positive relationship to a diverse extent, indicating that the related urinary metabolites could reflect the population's exposure to specific atmospheric PAHs. The findings also revealed that in the 16 selected countries, AirS indexes were positively correlated with ExpS indexes, implying that higher PAH levels in the air may lead to elevated metabolite urinary levels in general populations. Furthermore, lowering PAH air concentrations could reduce population internal PAH exposure, implying that strict PAH air regulation or emission would reduce health risks for general populations. Notably, this study was an ideal theoretical research based on proposed assumptions to some extent. Further research should focus on understanding exposure pathways, protecting vulnerable populations, and improving the PAH database to optimize PAH pollution control.

Sex-specific effect of urinary metabolites of polycyclic aromatic hydrocarbons on thyroid profiles: results from NHANES 2011-2012.

The current study aims to evaluate the associations between 10 urinary polycyclic aromatic hydrocarbon (PAH) metabolites and thyroid profiles. The levels of 10 PAH metabolites and thyroid profiles were obtained from National Health and Nutrition Examination Survey (NHANES) 2011-2012. Spearman analysis was utilized to evaluate the correlation coefficients among these 10 PAH metabolites. Multivariate linear and logistic regression models assessed the relationship between urinary PAH metabolite levels, thyroid hormones, and thyroid autoantibodies after adjusting potential confounders. Stratified analysis by gender was performed to evaluate sex-specific effect of urinary metabolites of PAH on thyroid profiles. One thousand six hundred forty-five eligible adult participants with complete research data were enrolled. Of note, the concentrations of the majority of urinary PAH metabolites were remarkedly higher in females compared with males. 2-hydroxyfluorene (2-FLU) was associated with higher total triiodothyronine (T3) levels in whole population (β = 2.113, 95% CI 0.339-3.888). In males, positive associations were observed in 1-hydroxynaphthalene (1-NAP) and free thyroxine (T4) (β = 0.0002, 95% CI 0.0000-0.0004). 2-FLU was also found positively associated with total T3 (β = 2.528, 95% CI 0.115-4.940) in male subjects. While in female participants, 2-hydroxynaphthalene (2-NAP) was associated with free T3 (β = 0.002, 95% CI 0.000-0.005). 2-FLU was associated with total T3 (β = 2.683, 95% CI 0.038-5.328), free T3 (β = 0.050, 95% CI 0.012-0.087), and total T4 (β = 0.195, 95% CI 0.008-0.382). 2-Hydroxyphenanthrene (2-OHP), 1-hydroxypyrene (1-HP), and 9-hydroxyfluorene (9-FLU) were all positively related to total T3 levels, and the corresponding coefficients were 16.504, 6.587, and 3.010. 9-FLU was also associated with free T3 (β = 0.049, 95% CI 0.008-0.090). No statistical significances were found between PAH metabolite levels and increased prevalence of increased thyroglobulin antibody (TgAb)/thyroid peroxidase antibody (TPOAb) when PAH metabolites were treated as continuous variables. Meanwhile, in the quartile analyses, increased prevalence of elevated TgAb was observed in participants with quartile 2 2-NAP compared with lowest quartile (OR = 1.753, 95% CI 1.021-3.008). Male subgroup analyses indicated that increased prevalence of elevated TgAb was observed in higher quartile of 1-NAP, 2-NAP, and 3-hydroxyfluorene (3-FLU). Increased prevalence of elevated TPOAb was associated with higher 2-NAP quartile. However, in subgroup analysis of females, no statistical significances were found between PAH quartiles and increased TgAb/TPOAb. Significant correlations were found among these 10 PAH metabolites. In conclusion, the cross-sectional study indicated that exposure to PAH might disturb the concentrations of thyroid hormones and thyroid autoantibodies. It is noteworthy that significant differences existed in males and females. Further prospective research is warranted to explore the causal relationship and underlying mechanism of PAH exposure on thyroid dysfunction.

Urinary polycyclic aromatic hydrocarbon metabolites are positively related to serum testosterone levels of males and serum estradiol levels of females among U.S. adults.

It has been reported for several years that polycyclic aromatic hydrocarbons (PAHs) could disturb human endocrine function. However, there is still a short of consistent conclusion about the relationship between PAH exposure and levels of sexual hormones. The aim of our study is to explore whether exposure to PAHs and how PAHs affect the levels of serum testosterone (T) and estradiol (E2) in adults, hoping to fulfill the knowledge gap. This study included adults aged 20 and above who participated in the National Health and Nutrition Examination Survey (NHANES) from 2011 to 2016. We included 10 PAH metabolites in this study. The levels of urinary PAH metabolites were log-transformed and divided into quartiles. The associations between PAH metabolites and both serum T levels of males and E2 levels of females were investigated using multivariate regression models. We furtherly calculated PAHs scores by sum of ranks across 10 PAHs metabolites, which represented the exposure levels of PAHs mixtures, and the association between PAHs scores and serum T and E2 levels were analyzed. A total of 4,654 subjects were included in this study, including 2,460 males and 2,194 females. After adjusting for confounders, 2-hydroxynapthalene and 3-hydroxyfluorene were positively associated with serum T levels of males (p-value for trend=0.047, and p-value for trend=0.006, respectively), while 1-hydroxyphenanthrene was positively associated with serum E2 levels of females (p-value for trend=0.013). In the adjusted models, no significant association was found between PAHs scores and either T levels of males or E2 levels of females (p-value for trend=0.615, and p-value for trend=0.241, respectively). This study showed urinary 2-hydroxynapthalene and 3-hydroxyfluorene were associated with increased T levels of males, and urinary 1-hydroxyphenanthrene was associated with increased E2 levels of females. The observed association indicated disrupting effects of PAH exposure on reproductive health.

PAHs exposure and its association with oxidative stress and neurotransmitter levels in coal miners

Objective: To learn the investigate of polycyclic aromatic hydrocarbons (PAHs) and to explore the association between PAHs exposure and oxidative stress' neurotransmitter levels in coal miners. Methods: A cross-sectional survey was conducted in 652 coal miners (239 in the underground first line group, 280 in the underground auxiliary group and 133 in the surface group) from April to June 2017. The levels of urinary monohydroxy PAHs metabolites (OH-PAHs) , oxidative stress and neurotransmitters in blood were determined. A linear regression model was used to evaluate the correlation between OH-PAHs and oxidative stress' neurotransmitter levels. The mediating role of oxidative stress between urinary OH-PAHs and neurotransmitters change was assessed by mediation analysis. Results: The levels of 2-hydroxynaphthalene (2-NAP) 、2-hydroxy uorene (2-FLU) 、1-hydroxypyrene (1-OHP) in urine OH-PAHs of coal miners in different workplaces were significantly different (H=33.64, 9.63, 26.82, P<0.01, =0.008, <0.01) . The levels of neurotransmitters [5-hydroxytryptamine (5-HT) , norepinephrine (NE) , epinephrine (E) , dopamine (DA) , acetylcholine (Ach) , acetylcholinesterase (AChE) ] and oxidative stress [malondialdehyde (MDA) (F=36.81, 15.58, 79.16, 179.58, 33.48, 67.63, 4.96, P<0.01) ] in the blood of three groups of coal miners were significantly different. After controlling the potential confounding factors, NE content was negatively correlated with 2-FLU level, and AChE activity was also negatively correlated with 1-OHP level (β=-134.99, 95% CI: -250.74~-19.23, P=0.02; β=-0.80, 95%CI: -1.54~-0.05, P=0.036) . Positive correlation was found between Ach content and 9-hydroxyphenanthrene (9-PHE) level, AChE activity was also positively correlated with 2-NAP level and 9-PHE level (β=0.96, 95%CI: 0.26~1.64, P=0.007; β=1.78, 95%CI: 0.75~2.82, P=0.001; β=0.77, 95%CI: 0.07~1.47, P=0.031) . In addition, superoxide dismutase activity was correlated with 1-OHP level and AChE activity (β=0.32, 95%CI: 0.02~0.62, P=0.034; β=-0.23, 95%CI: -0.43~-0.02, P=0.032) . Mediation analysis indicated that 1-OHP level may directly affect AChE activity (P<0.05) . Conclusion: The level of PAHs in underground coal miners is relatively higher, and may lead to changes of neurotransmitter levels. The mediating effect of oxidative stress has not been observed.

Polycyclic aromatic hydrocarbon exposure and DNA oxidative damage of workers in workshops of a petrochemical group.

The petrochemical industry has promoted the development of economy, while polycyclic aromatic hydrocarbons (PAHs) produced by the industry become the threat for environment and humans. Data on human occupational exposure in petrochemical industry are limited. In the present study, urinary hydroxylated PAH metabolites (OH-PAHs) and a biomarker of DNA oxidative damage (8-hydroxy-2'-deoxyguanosine (8-OHdG)) were measured in 546 workers of a petrochemical group in Northeast China, to investigate PAH exposure and related potential health risk. The concentrations of ∑9OH-PAH in all workers were 0.25-175μg/g Cre with a median value of 4.41μg/g Cre. Metabolites of naphthalene were the predominant compounds. The levels of PAH metabolites were significantly different for workers with different jobs, which were the highest for recycling workers (13.7μg/g Cre) and the lowest for agency managers (5.12μg/g Cre). Besides, higher levels of OH-PAHs were usually found in males and older workers. There was a dose-response relationship between levels of 8-OHdG and ∑9OH-PAHs (p<0.01). No difference was observed in concentrations of 8-OHdG for workers of different gender or ages, work history as well as noise. Furthermore, workers simultaneously exposed to other potential pollutants and higher levels of ∑9OH-PAH had significantly higher levels of 8-OHdG compared with those in the corresponding subgroups. Our results suggested that exposure to PAHs or co-exposure to PAHs and potential toxics in the petrochemical plant may cause DNA damage. We call for more researches on the associations among noise, chemical pollution and oxidative stress to workers in the real working environment.

The Association between Urinary Polycyclic Aromatic Hydrocarbons Metabolites and Type 2 Diabetes Mellitus

Polycyclic aromatic hydrocarbons (PAHs) are considered to be endocrine disruptors. In this study, the evidence on the association between PAHs and diabetes was systematically reviewed. PubMed, EMBASE, and ISI Web of Science were systematically searched for studies reporting the association between PAHs and diabetes. Of the 698 articles identified through the search, nine cross-sectional studies were included. Seven were conducted in the general population and two in coke oven workers. Fixed-effects and random-effects models were used to calculate the total effect. Subgroup analysis was further carried out according to the types of PAH metabolites. The results showed that the odds of diabetes were significantly higher for the highest category of urinary naphthalene (NAP), fluorine (FLU), phenanthrene (PHEN), and total mono-hydroxylated (OH-PAH) metabolites compared to the lowest category. The pooled odds ratios (OR) and 95% confidence intervals (CI) were 1.52 (95%CI: 1.19, 1.94), 1.53 (95%CI: 1.36, 1.71), 1.43 (95%CI: 1.28, 1.60), and 1.49 (95%CI: 1.07, 2.08), respectively. In coke oven workers, 4-hydroxyphenanthrene (4-OHPh) was significantly correlated with an increased risk of diabetes. Exposure measurements, outcome definitions, and adjustment for confounders were heterogeneous between studies. The results of the current study demonstrate a potentially adverse effect of PAHs on diabetes. Further mechanistic studies and longitudinal studies are needed to confirm whether PAH metabolite levels are causative, and hence associative, with increased diabetes incidences.

Exposure to polycyclic aromatic hydrocarbons and nicotine, and associations with sperm DNA fragmentation.

BackgroundTobacco smoking has been reported to cause DNA fragmentation and has been suggested to cause mutations in spermatozoa. These effects have been ascribed to the action of polycyclic aromatic hydrocarbons (PAH) present in the smoke. Simultaneously, DNA fragmentation has been associated with mutagenesis.ObjectiveThe aim of this study was to investigate whether levels of urinary biomarkers of PAH and nicotine exposure were associated with sperm DNA fragmentation.MethodsIn the urine of 381 men recruited from two cohorts of young men (17–21 years old) from the general Swedish population, the PAH metabolites 1‐hydroxypyrene and 2‐hydroxyphenanthrene, as well as the nicotine metabolite cotinine, were measured. The sperm DNA fragmentation index (DFI) was analysed using the sperm chromatin structure assay. Associations between the DFI, and PAH metabolite levels as continuous variables as well as in quartiles, were studied by general linear models adjusted for abstinence time. A similar analysis was carried out for cotinine levels, according to which the men were categorised as “non‐smoking” (n = 216) and “smoking” (n = 165).ResultsNo association was found between levels of any of the three biomarkers and DFI, either as a continuous variable (p = 0.87–0.99), or when comparing the lowest and the highest quartiles (p = 0.11–0.61). The same was true for comparison of men categorised as non‐smoking or smoking (DFI 11.1% vs. 11.8%, p = 0.31).DiscussionWe found no evidence of PAH or nicotine exposure to be associated with DFI, which does not exclude that these exposures may have other effects on sperm DNA.ConclusionIn these young men, levels of biomarkers of nicotine and PAH exposure were not associated with DFI.

Associations of Bitumen Fumes with Lymphocyte Subsets and Cytokines Expression in the Peripheral Blood of Exposed Workers

The present study aimed to investigate the distribution of lymphocyte subsets and cytokines expression in the peripheral blood of bitumen fumes-exposed workers. In this study, 129 workers from molding and roasting workshops were recruited as the exposed group and 99 office and quality inspection staff were chosen as the control. The polycyclic aromatic hydrocarbons (PAHs) levels of bitumen fumes in individual and fixed-point air samples and the urinary levels of 1-hydroxypyrene (1-OH-P), 1-hydroxynaphthols (1-OH-N) and 2-hydroxynaphthols (2-OH-N) in workers were measured using High Performance Liquid Chromatography. The lymphocyte subsets and serum cytokines concentrations were analyzed by flow cytometry and cytometric bead array, respectively. The median values of PAHs were 0.08 mg/m3 for permissible concentration-time weighted average and 0.12 mg/m3 for permissible concentration-short term exposure (PC-STEL) in molding and roasting workshops, which were higher than that in the control area (< 0.01 mg/m3). Multivariate linear regression models were used to adjust for influential covariates, including age, gender, work age, smoking status, and alcohol consumptions. After adjusting for these covariates, we compared levels of urinary PAHs metabolites, the percentages of lymphocyte subsets, and serum cytokines concentrations between the two groups. The 1-OH-P, 1-OH-N, and 2-OH-N levels in the urine of bitumen fumes exposed workers were significantly higher than that in the controls (P < 0.05). Compared with the control group, the percentage of the natural killer (NK) cell (CD56+ cell) was significantly increased in the exposed group (P < 0.001). There was a significant decrease in the percentages of CD3+ T cell, CD4+ T cell, and CD8+ T cell in the exposed group compared to the control (P < 0.001). The serum levels of interleukin-1β (IL-1β) and IL-6 in bitumen fumes exposed workers were significantly higher than that of the controls (P < 0.05). Moreover, positive correlations were observed between the serum levels of IL-1β, IL-6, and urinary 1-OH-P levels in bitumen fumes-exposed workers, respectively (P < 0.05). There were no significant differences in the serum levels of IL-8, tumor necrosis factor-α (TNF-α), macrophage inflammatory protein-1β (MIP-1β) and monocyte chemotactic protein-1 (MCP-1) between the exposed group and the control group (P > 0.05). Our study suggested that low dose of bitumen fumes exposure could decrease the percentage of T cell, increase the percentage of NK cell and stimulate the release of serum IL-1β and IL-6 in the peripheral blood of exposed workers. The serum levels of IL-1β and IL-6 were positive correlated with the urinary 1-OH-P levels in bitumen fumes exposed workers. These results may inform the search for potential effective biomarkers and provide evidences for early health monitoring in workers occupationally exposed to bitumen fumes.

Proximity to traffic and exposure to polycyclic aromatic hydrocarbons in relation to Attention Deficit Hyperactivity Disorder and conduct disorder in U.S. children.

Traffic related air pollution (TRAP) and its component polycyclic aromatic hydrocarbons (PAHs) may be neurotoxic in children. There is limited research on postnatal exposure to TRAP and PAHs and child neurodevelopment. We linked data from the U.S. NHANES 2001-2004 with the National Highway Planning Network 2005 to examine the proximity to major roads (highway or urban/rural principal arterials), urinary PAH metabolites, and diagnosis of Attention Deficit Hyperactivity Disorder (ADHD) and Conduct Disorder (CD) based on Diagnostic Interview Schedule for Children (C-DISC) in 1253 children aged 8-15 years. We calculated odds ratios (ORs) and 95% Confidence Intervals (CIs) for ADHD and CD by traffic proximity and PAH exposures using logistic regression adjusted for confounders. Higher ADHD prevalence was observed among children living <500m (9.86%) compared to those ≥500m (3.84%) from a major road. Prevalence of children with CD was comparable (<500m: 2.51% and ≥500m: 2.43%). We found little difference in urinary PAH metabolite levels between children living near major roads and those who did not. Children living <500m from a major road had a non-significant OR of 2.06 (95% CI 0.85-5.03) for ADHD diagnosis. Children living on ≥2 major roads within 500m of a highway had a non-significant OR of 2.27 (95% CI 0.71-7.26) for ADHD diagnosis. There was no association between proximity to major roads and CD diagnosis. We found living close to a major road was not associated with increased PAH levels. We did not find statistically significant relation between proximity to a major road or urinary PAH metabolite levels and ADHD or CD diagnosis in this cross-sectional analysis. Prospective studies are needed for the investigation of postnatal TRAP exposure and ADHD and CD diagnosis.

Ambient particulate matter compositions and increased oxidative stress: Exposure-response analysis among high-level exposed population

BackgroundOxidative stress has been suggested to be one of the key drivers of health impact of particulate matter (PM). More studies on the oxidative potential of PM alone, but fewer studies have comprehensively evaluated the effects of external and internal exposure to PM compositions on oxidative stress in population. ObjectiveTo comprehensively investigate the exposure–response relationship between PM and its main compositions with oxidative stress indicators. MethodsWe conducted a cross-sectional study including 768 participants exposed to particulates. Environmental levels of fine particulate matter (PM2.5), polycyclic aromatic hydrocarbons (PAHs) and metals in PM were measured, and urinary levels of PAHs metabolites and metals were measured as internal dose, respectively. Multivariable linear regression models were used to analyze the correlations of PM exposure and urinary levels of 8-hydroxy-2́′-deoxyguanosine (8-OHdG), and 8-iso-prostaglandin-F2α (8-iso-PGF2α) and malondialdehyde (MDA). ResultsThe concentration of both PM2.5 and total PAHs was significantly correlated with increased urinary 8-OHdG, 8-iso-PGF2α and MDA levels (all p < 0.05). The levels of 4 essential metals all showed significant exposure–response increase in urinary 8-OHdG in both current and non-current smokers (all p < 0.05); ambient selenium, cobalt and zinc were found to be significantly correlated with urinary 8-iso-PGF2α (p = 0.002, 0.003, 0.01, respectively); only selenium and cobalt were significantly correlated with urinary MDA (p < 0.001, 0.01, respectively). Furthermore, we found each one-unit increase in urinary total OH-PAHs generated a 0.32 increase in urinary 8-OHdG, a 0.22 increase in urinary 8-iso-PGF2α and a 0.19 increase in urinary MDA (all p < 0.001). Furthermore, it was found that the level of 12 urinary metals all showed significant and positive correlations with three oxidative stress biomarkers in all subjects (all p < 0.001). ConclusionsOur systematic molecular epidemiological study showed that particulate matter components could induce increased oxidative stress on DNA and lipid. It may be more important to monitor and control the harmful compositions in PM rather than overall particulate mass.

Trophic Transfer of Micropollutants and Their Metabolites in an Urban Riverine Food Web.

Trophic magnification factors (TMFs, i.e., the average change in the log-concentration of a pollutant per trophic level) have been extensively assessed for the so-called persistent organic pollutants, especially organochlorine pesticides (OCPs) and polychlorinated biphenyls (PCBs), which are biomagnified along the food web. In contrast, trophic dilution was documented for pollutants with a high metabolic conversion rate, such as phthalate plasticizers and polycyclic aromatic hydrocarbons (PAHs). However, the fate of their metabolites across the food web has been rarely investigated. In this comparative study, the trophodynamics of 104 micropollutants and 25 of their metabolites were investigated in a freshwater food web from the urban Orge River, France. Trophic levels were determined using stable isotopes. Pyrethroid pesticides and their metabolites were not detected. As predicted, PCBs and OCPs biomagnified (TMF >1), while all chlorinated paraffins (CPs), PAHs, and phthalates underwent a trophic dilution (TMF <1). TMFs significantly decreased with a metabolic transformation rate and increased with hydrophobicity. The levels of PAH or phthalate metabolites were not significantly correlated with trophic levels or underwent a trophic dilution. This study highlighted that the relative contribution of metabolite levels in TMF values calculated for both parent compound and its metabolite(s) is weak compared to TMF values of the parent compound only in a riverine food web.

Polycyclic aromatic hydrocarbon exposure and atherosclerotic cardiovascular disease risk in urban adults: The mediating role of oxidatively damaged DNA

Polycyclic aromatic hydrocarbon (PAH) exposure has been considered a risk factor for cardiovascular diseases (CVD), whereas possible mechanisms for this association have not been fully understood. This study focused on exploring the potential effect of oxidatively damaged DNA on the relationships between PAH exposure and the 10-year atherosclerotic CVD (ASCVD) risk. Urinary levels of monohydroxy PAH metabolites (OH-PAHs) and 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG, the typical biomarker for oxidatively damaged DNA) were measured among 3052 subjects in the baseline of the Wuhan-Zhuhai cohort. The relationships between urinary OH-PAHs, 8-oxodG and 10-year risk of ASCVD were analyzed by linear mixed models and logistic regression models, respectively. The mediation analysis was further applied to explore the role of 8-oxodG in the relationship between urinary OH-PAHs and 10-year ASCVD risk. After controlling for potential confounders, the log-transformed level of total urinary low molecular weight OH-PAHs (∑LMW OH-PAHs) was significantly associated with an elevated risk of 10-year ASCVD [odds ratio (OR) = 1.222, 95% confidence interval (CI): 1.065–1.402]. More specifically, significantly positive dose-response relationships between total urinary hydroxynaphthalene (∑OHNa), hydroxyfluorene (∑OHFlu), hydroxyphenanthrene (∑OHPh) and 10-year ASCVD risk were observed (all P for trend <0.05). We also found positive relationships between urinary OH-PAH levels and 8-oxodG, as well as between urinary 8-oxodG levels and 10-year risk of ASCVD. Moreover, mediation analyses indicated that urinary 8-oxodG mediated 14.49%, 12.62% and 10.55% of the associations between urinary ∑LMW OH-PAHs, ∑OHNa, ∑OHFlu and 10-year ASCVD risk, respectively. These findings suggest that the oxidatively damaged DNA pathway may be a possible mechanism underlying PAH-associated ASCVD risk elevation.

Neurobehavioral performance of PAH exposure in male coal miners in Shanxi, China: a cross-sectional study.

Coal miners are exposed to polycyclic aromatic hydrocarbons (PAHs), a group of neurotoxicants formed and released during incomplete combustion of coal. High levels of anxiety and depression have been reported in coal miners, but little is known about neurobehavioral functions in populations that are occupationally exposed to PAHs. We tested neurobehavioral performance in coal miners and correlated it with levels of urinary markers of PAH exposure. Levels of urinary PAH metabolites were measured in 652 male coal miners as an indicator of exposure. Subjects were divided into a high-exposure group and a low-exposure group based on the median level of total PAH metabolites. A neurobehavioral core test battery and a questionnaire were used to assess neurobehavioral performance and collect demographic information, respectively. The median level of total PAH metabolites in urine was 4.88μmol/mol creatinine. Highly exposed workers exhibited more fatigue-inertia than less-exposed workers (p < 0.05), and had lower scores in forward digit span, digit symbol, and Benton visual retention tests (p < 0.05). Multiple linear regression indicated that age, education, and shift work were significantly correlated with test scores. PAH exposure may be associated with neurobehavioral alterations, which should be monitored in coal miners to prevent neurobehavioral disorders.