ABSTRACT
BACKGROUND: Developmental dyslexia, a complex neurodevelopmental disorder, not only affects children's academic performance but is also associated with increased healthcare costs, lower employment rates, and reduced productivity. The pathogenesis of dyslexia remains unclear and it is generally considered to be caused by the overlap of genetic and environmental factors. Systematically exploring the close relationship between exposure to environmental compounds and susceptibility genes in the development of dyslexia is currently lacking but high necessary. METHODS: In this study, we systematically compiled 131 publicly reported susceptibility genes for dyslexia sourced from DisGeNET, OMIM, and GeneCards databases. Comparative Toxicogenomics Database database was used to explore the overlap between susceptibility genes and 95 environmental compounds, including metals, persistent organic pollutants, polycyclic aromatic hydrocarbons, and pesticides. Chemical bias towards the dyslexia risk genes was taken into account in the observation/expectation ratios > 1 and the corresponding P value obtained by hypergeometric probability test. RESULTS: Our study found that the number of dyslexia risk genes targeted by each chemical varied from 1 to 109. A total of 35 chemicals were involved in chemical reactions with dyslexia-associated genes, with significant enrichment values (observed/expected dyslexia risk genes) ranging from 1.147 (Atrazine) to 66.901 (Dibenzo(a, h)pyrene). CONCLUSION: The results indicated that dyslexia-associated genes were implicated in certain chemical reactions. However, these findings are exploratory, and further research involving animal or cellular experiments is needed.
Subject(s)
Dyslexia , Environmental Pollutants , Genetic Predisposition to Disease , Humans , Dyslexia/genetics , Genetic Predisposition to Disease/genetics , Environmental Pollutants/adverse effects , Polycyclic Aromatic Hydrocarbons/adverse effects , ToxicogeneticsABSTRACT
Low-grade cervical intraepithelial neoplasia (CIN1) is an early stage of cervical cancer development. Previously, we reported that exposure to polycyclic aromatic hydrocarbons (PAHs) increases the risk of cervical precancerous lesions, especially in females with a high-risk human papillomavirus (HR-HPV) infection. However, the effects of PAHs on CIN1 progression remain unclear. A community-based prospective cohort study was conducted to evaluate the role of exposure to PAHs in the progression of CIN1. A total of 564 patients diagnosed with CIN1 were followed-up at 6, 12, and 24 months, post-diagnosis, to determine CIN1 reversion, persistence, and progression. Exposure to PAHs was determined by the urine 1-hydroxipayrene (1-OHP) level. Our results showed that the 1-OHP level was significantly higher in patients with CIN1 persistence/progression than in those with reversion (P < .05). High exposure to PAHs increased the risk of CIN1 persistence/progression, with hazard ratios (HR), 95% confidence intervals (CI) of (1.62, 1.24-2.67), (1.98, 1.42-2.75), and (2.37, 1.61-3.49) at 6, 12, and 24 months, post-diagnosis, respectively. The effect was enhanced with HR-HPV positivity, as determined at 6 (1.82, 1.24-2.67), 12 (3.02, 1.74-5.23), and 24 (2.51, 1.48-4.26) months, post-diagnosis. Moreover, the predictive value of exposure to PAHs for CIN1 persistence/progression was higher in HR-HPV-positive patients than in HR-HPV-negative patients. The results revealed that exposure to PAHs facilitated the malignant progression of CIN1 and hindered its reversal, particularly in patients with HR-HPV infection. Our findings provide novel insights into early prevention and intervention targeting the initiation and progression of cervical neoplasia.
Subject(s)
Disease Progression , Polycyclic Aromatic Hydrocarbons , Uterine Cervical Dysplasia , Uterine Cervical Neoplasms , Humans , Female , Uterine Cervical Dysplasia/epidemiology , Uterine Cervical Dysplasia/virology , Uterine Cervical Dysplasia/pathology , Polycyclic Aromatic Hydrocarbons/adverse effects , China/epidemiology , Adult , Uterine Cervical Neoplasms/virology , Uterine Cervical Neoplasms/epidemiology , Uterine Cervical Neoplasms/pathology , Middle Aged , Prospective Studies , Papillomavirus Infections/virology , Papillomavirus Infections/complications , Papillomavirus Infections/epidemiology , Cohort Studies , Environmental Exposure/adverse effectsABSTRACT
PURPOSE: Polycyclic aromatic hydrocarbons (PAHs) represent a class of ubiquitous pollutants recognized as established human carcinogens and endocrine-disrupting chemicals. PAHs have seldom been modeled at the population-level in epidemiological studies. Fluoranthene is a prevalent PAH in urban settings and correlates with the occurrence of other PAHs. The purpose of this study was to evaluate associations between long-term residential exposure to ambient PAHs and breast cancer risk, both pre- and post-menopausal, in Canada. METHODS: Using the National Enhanced Cancer Surveillance System (NECSS), a national-scale Canadian population-based case-control study, annual fluoranthene exposures were estimated using the GEM-MACH-PAH chemical transport model on the basis of geocoded residential histories throughout a 20-year exposure window. Odds ratios (ORs) and 95% confidence intervals (CIs) controlling for potential confounders were estimated using logistic regression. Separate analyses were conducted for Ontario and national samples given a finer-resolution exposure surface and additional risk factor information available for Ontario. RESULTS: Positive associations were observed between fluoranthene exposure and premenopausal breast cancer, with inconsistent findings for postmenopausal breast cancer. For premenopausal breast cancer, adjusted ORs of 2.48 (95% CI: 1.29, 4.77) and 1.59 (95% CI: 1.11, 2.29) were observed when comparing the second highest category of exposure to the lowest, among the Ontario and national samples, respectively. For postmenopausal breast cancer, adjusted ORs were 1.10 (95% CI: 0.67, 1.80) and 1.33 (95% CI: 1.02, 1.73). Associations for the highest level of exposure, across both samples and menopausal strata, were non-significant. CONCLUSION: This study provides support for the hypothesis that ambient PAH exposures increase the risk of premenopausal breast cancer.
Subject(s)
Breast Neoplasms , Environmental Exposure , Polycyclic Aromatic Hydrocarbons , Humans , Female , Case-Control Studies , Breast Neoplasms/epidemiology , Breast Neoplasms/chemically induced , Breast Neoplasms/etiology , Polycyclic Aromatic Hydrocarbons/adverse effects , Polycyclic Aromatic Hydrocarbons/toxicity , Middle Aged , Canada/epidemiology , Adult , Environmental Exposure/adverse effects , Risk Factors , Aged , Fluorenes , Ontario/epidemiology , Odds RatioABSTRACT
Phthalates (PAEs) and polycyclic aromatic hydrocarbons (PAHs) are frequently detected in females of reproductive age. Many studies have found that environmental PAE and PAH levels are independent risk factors for gestational hypertension. However, exposure to both components is a more realistic scenario. To better assess the health effects of PAEs and PAHs in pregnant women, we explored the associations of exposure to both individual and combined PAEs and PAHs with gestational hypertension. This nested case-control study was a component of a prospective cohort study conducted in Beijing, China. We included 206 women with gestational hypertension and 214 pregnant controls. We used gas chromatography/tandem mass spectrometry (GC-MS/MS) to detect 8 PAEs and 13 PAHs in > 80 % of all collected hair samples. Multiple linear regression models were employed to test the individual associations between each component and gestational hypertension. A quantile-based g-computation (qgcomp) model and a weighted quantile sum (WQS) regression model were used to estimate whether exposure to both PAEs and PAHs increased the risk of gestational hypertension. The individual exposure analyses revealed that diethyl phthalate (DEP), diisobutyl phthalate (DIBP) (both PAEs), benzo(k)fluoranthene (BKF), anthracene, (ANT), and benzo(a)pyrene (BAP) (all PAHs) were positively associated with increased risk of gestational hypertension. In mixed-effect analyses, the qgcomp model indicated that co-exposure to PAEs and PAHs increased the risk of gestational hypertension (odds ratio = 2.01; 95 % confidence interval: 1.02, 3.94); this finding was verified by the WQS regression model. Our findings support earlier evidence that both PAEs and PAHs increase the risk of gestational hypertension, both individually and in combination. This suggests that reductions in exposure to endocrine system-disrupting chemicals such as PAEs and PAHs might reduce the risk of gestational hypertension.
Subject(s)
Hypertension, Pregnancy-Induced , Polycyclic Aromatic Hydrocarbons , Humans , Female , Pregnancy , Polycyclic Aromatic Hydrocarbons/adverse effects , Polycyclic Aromatic Hydrocarbons/analysis , Tandem Mass Spectrometry , Hypertension, Pregnancy-Induced/epidemiology , Case-Control Studies , Prospective Studies , China/epidemiologyABSTRACT
BACKGROUND AND AIM: Studies suggest prenatal exposure to polycyclic aromatic hydrocarbons (PAHs) may influence wheezing or asthma in preschool-aged children. However, the impact of prenatal PAH exposure on asthma and wheeze in middle childhood remain unclear. We investigated these associations in socio-demographically diverse participants from the ECHO PATHWAYS multi-cohort consortium. METHODS: We included 1,081 birth parent-child dyads across five U.S. cities. Maternal urinary mono-hydroxylated PAH metabolite concentrations (OH-PAH) were measured during mid-pregnancy. Asthma at age 8-9 years and wheezing trajectory across childhood were characterized by caregiver reported asthma diagnosis and asthma/wheeze symptoms. We used logistic and multinomial regression to estimate odds ratios of asthma and childhood wheezing trajectories associated with five individual OH-PAHs, adjusting for urine specific gravity, various maternal and child characteristics, study site, prenatal and postnatal smoke exposure, and birth year and season in single metabolite and mutually adjusted models. We used multiplicative interaction terms to evaluate effect modification by child sex and explored OH-PAH mixture effects through Weighted Quantile Sum regression. RESULTS: The prevalence of asthma in the study population was 10%. We found limited evidence of adverse associations between pregnancy OH-PAH concentrations and asthma or wheezing trajectories. We observed adverse associations between 1/9-hydroxyphenanthrene and asthma and persistent wheeze among girls, and evidence of inverse associations with asthma for 1-hydroxynathpthalene, which was stronger among boys, though tests for effect modification by child sex were not statistically significant. CONCLUSIONS: In a large, multi-site cohort, we did not find strong evidence of an association between prenatal exposure to PAHs and child asthma at age 8-9 years, though some adverse associations were observed among girls.
Subject(s)
Asthma , Phenanthrenes , Polycyclic Aromatic Hydrocarbons , Prenatal Exposure Delayed Effects , Child , Pregnancy , Male , Female , Child, Preschool , Humans , Longitudinal Studies , Polycyclic Aromatic Hydrocarbons/adverse effects , Prenatal Exposure Delayed Effects/chemically induced , Prenatal Exposure Delayed Effects/epidemiology , Respiratory Sounds , Asthma/chemically induced , Asthma/epidemiologyABSTRACT
BACKGROUND: Polycyclic aromatic hydrocarbons (PAHs) are prevalent organic pollutants in the environment; however, limited research has been conducted to explore their potential effects on sleep disorders. This study aims to investigate the relationship between single and mixed PAHs exposures and sleep disorders. METHODS: This study analyzed National Health and Nutrition Examination Survey (NHANES) data from 2005 to 2016, involving 7730 adult participants. To examine the relationship between PAHs exposure and sleep disorders, we employed survey-weighted multivariate logistic regression models and restricted cubic spline (RCS) models to evaluate single PAHs exposure. Additionally, we employed three mixed-exposure models to examine the relationship between combined PAHs exposure and sleep disorders. RESULTS: After adjusting for covariates, our analyses revealed positive associations between several urinary PAHs metabolites (1-hydroxynaphthalene (1-NAP), 2-NAP, 3-hydroxyfluorene (3-FLU), 2-FLU, and 1-hydroxypyrene (1-PYR)) and sleep disturbance. Consistency across various analytical methods underscores a discernible positive correlation between simultaneous exposure to PAHs and sleep disorders. This association is predominantly influenced by the presence of NAP and FLU. Remarkably, a positive relationship between combined PAHs exposure and sleep disorders emerged within the younger and middle-aged demographic but did not manifest within the elderly population. CONCLUSION: In conclusion, our study provides new epidemiological evidence suggesting that both single and mixed PAHs exposures may increase the risk of sleep disorders. Further prospective investigations are necessary to validate these findings.
Subject(s)
Polycyclic Aromatic Hydrocarbons , Adult , Middle Aged , Humans , Aged , Polycyclic Aromatic Hydrocarbons/adverse effects , Nutrition Surveys , Biomarkers , Logistic ModelsABSTRACT
BACKGROUND: There is suggestive epidemiological evidence that maternal dietary polycyclic aromatic hydrocarbons (PAH) may increase the risk of adverse birth outcomes. We sought to summarize the available evidence on the effect of dietary PAH exposure on birth outcomes. METHODS: PubMed and Scopus databases were systematically searched from inception up to November 2022. Studies were included if they were original articles, were conducted in a human population, assessed dietary PAH consumption, and investigated the relationship between dietary PAH consumption and any adverse birth outcomes. Risk of bias in the included studies was assessed qualitatively and quantitatively. A random effects model was used to compute summary effect estimates in the meta-analysis. RESULTS: Six observational studies (five prospective cohort studies, and one prevalence case-control study) were included. The included studies assessed dietary PAH exposure using dietary questionnaires. Information on the outcomes of interest was obtained from medical records. Three of the included studies were rated as good quality with the remaining three studies rated as fair quality. One study was considered as having low risk of bias for selection, information and confounding bias. Dietary PAH consumption was associated with 5.65g [95% confidence interval (CI): -16.36, 5.06] and 0.04cm (95% CI: -0.08, 0.01) reductions in birth weight and birth length, respectively, and an increase in head circumference [effect size (ES)=0.001; 95% CI: -0.003, 0.005]. The CI of all the summary effect estimates, however, included the null value. In the sensitivity analysis that included only studies that assessed dietary PAH exposure as the primary exposure of interest, dietary PAH consumption was associated with much higher reductions in birth weight (ES=-14.61; 95% CI: -21.07, -8.15) and birth length (ES=-0.06; 95% CI: -0.1, -0.03). High statistical heterogeneity was observed in the birth weight and birth length analysis and in the head circumference sensitivity analysis. DISCUSSION: The body of epidemiological evidence suggests that maternal dietary PAH exposure is associated with reduced fetal growth, measured as birth weight and length. There was considerable heterogeneity in the measurement of PAH exposure among the included studies. Also, nonstandardized and validated dietary questionnaires were employed by a majority of the included studies with potential exposure misclassification. These issues are likely to impact the summary effect estimates computed and underscores the need for high-quality epidemiological studies with improved exposure assessment and adequate confounding control to strengthen the evidence base. https://doi.org/10.1289/EHP12922.
Subject(s)
Polycyclic Aromatic Hydrocarbons , Pregnancy Complications , Female , Humans , Birth Weight , Case-Control Studies , Polycyclic Aromatic Hydrocarbons/adverse effects , Prospective StudiesABSTRACT
INTRODUCTION: Prenatal exposure to environmental chemicals may be associated with allergies later in life. We aimed to examine the association between prenatal dietary exposure to mixtures of chemicals and allergic or respiratory diseases up to age 5.5 y. METHODS: We included 11,638 mother-child pairs from the French "Étude Longitudinale Française depuis l'Enfance" (ELFE) cohort. Maternal dietary exposure during pregnancy to eight mixtures of chemicals was previously assessed. Allergic and respiratory diseases (eczema, food allergy, wheezing and asthma) were reported by parents between birth and age 5.5 years. Associations were evaluated with adjusted logistic regressions. Results are expressed as odds ratio (OR[95%CI]) for a variation of one SD increase in mixture pattern. RESULTS: Maternal dietary exposure to a mixture composed mainly of trace elements, furans and polycyclic aromatic hydrocarbons (PAHs) was positively associated with the risk of eczema (1.10 [1.05; 1.15]), this association was consistent across sensitivity analyses. Dietary exposure to one mixture of pesticides was positively associated with the risk of food allergy (1.10 [1.02; 1.18]), whereas the exposure to another mixture of pesticides was positively but slightly related to the risk of wheezing (1.05 [1.01; 1.08]). This last association was not found in all sensitivity analyses. Dietary exposure to a mixture composed by perfluoroalkyl acids, PAHs and trace elements was negatively associated with the risk of asthma (0.89 [0.80; 0.99]), this association was consistent across sensitivity analyses, except the complete-case analysis. CONCLUSION: Whereas few individual chemicals were related to the risk of allergic and respiratory diseases, some consistent associations were found between prenatal dietary exposure to some mixtures of chemicals and the risk of allergic or respiratory diseases. The positive association between trace elements, furans and PAHs and the risk of eczema, and that between pesticides mixtures and food allergy need to be confirmed in other studies. Conversely, the negative association between perfluoroalkyl acids, PAHs and trace elements and the risk of asthma need to be further explored.
Subject(s)
Asthma , Eczema , Fluorocarbons , Food Hypersensitivity , Pesticides , Polycyclic Aromatic Hydrocarbons , Respiration Disorders , Respiratory Tract Diseases , Trace Elements , Female , Pregnancy , Humans , Child, Preschool , Dietary Exposure/adverse effects , Respiratory Sounds , Asthma/chemically induced , Asthma/epidemiology , Eczema/chemically induced , Eczema/epidemiology , Furans , Polycyclic Aromatic Hydrocarbons/adverse effectsABSTRACT
OBJECTIVE: This study aimed to investigate the effects of polycyclic aromatic hydrocarbon (PAH) exposure and telomere length on lipids in coal miners. METHODS: Basic personal information of 637 coal miners was collected by questionnaire survey. Logistic regression, the Bayesian kernel machine regression model, and weighted quantile sum regression were used to analyze the effects of PAH metabolites and telomere length and their interactions on blood lipids. RESULTS: High exposure to 9-hydroxyphenanthrene (OR = 1.586, 95% CI: 1.011-2.487) and telomere shortening (OR = 1.413, 95% CI: 1.005-1.985) were associated with dyslipidemia. Weighted quantile sum results showed that 9-hydroxyphenanthrene accounted for the largest proportion of dyslipidemia (weight = 0.66). The interaction results showed that high 9-hydroxyphenanthrene exposure and short telomeres were risk factors for dyslipidemia in coal miners (OR = 2.085, 95% CI: 1.121-3.879). Conclusions: Our findings suggest that 9-hydroxyphenanthrene and shorter telomeres are risk factors for dyslipidemia, and their interaction increases the risk of dyslipidemia.
Subject(s)
Dyslipidemias , Phenanthrenes , Polycyclic Aromatic Hydrocarbons , Humans , Polycyclic Aromatic Hydrocarbons/adverse effects , Bayes Theorem , Telomere , Coal , BiomarkersABSTRACT
BACKGROUND: Studying carcinogens in tobacco and nontobacco sources may be key to understanding the pathogenesis and geographic distribution of esophageal cancer. METHODS: The Golestan Cohort Study has been conducted since 2004 in a region with high rates of esophageal squamous cell carcinoma. For this nested study, the cases comprised of all incident cases by January 1, 2018; controls were matched to the case by age, sex, residence, time in cohort, and tobacco use. We measured urinary concentrations of 33 exposure biomarkers of nicotine, polycyclic aromatic hydrocarbons, volatile organic compounds, and tobacco-specific nitrosamines. We used conditional logistic regression to calculate odds ratios (ORs) and 95% confidence intervals for associations between the 90th vs the 10th percentiles of the biomarker concentrations and incident esophageal squamous cell carcinoma. RESULTS: Among individuals who did not currently use tobacco (148 cases and 163 controls), 2 acrolein metabolites, 2 acrylonitrile metabolites, 1 propylene oxide metabolite, and one 1,3-butadiene metabolite were significantly associated with incident esophageal squamous cell carcinoma (adjusted odds ratios between 1.8 and 4.3). Among tobacco users (57 cases and 63 controls), metabolites of 2 other volatile organic compounds (styrene and xylene) were associated with esophageal squamous cell carcinoma (OR = 6.2 and 9.0, respectively). In tobacco users, 2 tobacco-specific nitrosamines (NNN and N'-Nitrosoanatabine) were also associated with esophageal squamous cell carcinoma. Suggestive associations were seen with some polycyclic aromatic hydrocarbons (especially 2-hydroxynaphthalene) in nonusers of tobacco products and other tobacco-specific nitrosamines in tobacco users. CONCLUSION: These novel associations based on individual-level data and samples collected many years before cancer diagnosis, from a population without occupational exposure, have important public health implications.
Subject(s)
Esophageal Neoplasms , Esophageal Squamous Cell Carcinoma , Nitrosamines , Polycyclic Aromatic Hydrocarbons , Volatile Organic Compounds , Humans , Biomarkers , Cohort Studies , Esophageal Neoplasms/epidemiology , Esophageal Neoplasms/etiology , Esophageal Squamous Cell Carcinoma/epidemiology , Esophageal Squamous Cell Carcinoma/etiology , Incidence , Polycyclic Aromatic Hydrocarbons/adverse effects , Volatile Organic Compounds/adverse effectsABSTRACT
AIM: To explore the association between polycyclic aromatic hydrocarbons (PAHs) (measured using urinary metabolites) and periodontitis using data from the National Health and Nutrition Examination Survey 2009-2014. MATERIALS AND METHODS: Weighted binary logistic regression, Bayesian kernel machine regression (BKMR) and weighted quantile sum (WQS) regression were used to evaluate independent and joint associations between the six urinary monohydroxylated metabolites of PAHs (OH-PAHs) and periodontitis. RESULTS: In all, 3413 participants were included in this study. All six urinary OH-PAHs were present at higher levels in the periodontitis group compared with the non-periodontitis group (p < .001). Fully adjusted multivariable logistic regressions showed positive associations between the six urinary OH-PAHs and periodontitis (p < .05). Higher concentrations of OH-PAHs were also positively associated with attachment loss, periodontal pocket depth (PPD) and the number of tooth loss. BKMR and WQS regression yielded similar positive associations between OH-PAH mixtures and periodontitis. CONCLUSIONS: PAHs and their mixture are positively associated with periodontitis, which may provide novel insights into periodontitis prevention from an environmental exposure perspective.
Subject(s)
Periodontitis , Polycyclic Aromatic Hydrocarbons , Humans , Bayes Theorem , Nutrition Surveys , Periodontitis/epidemiology , Periodontal Pocket , Polycyclic Aromatic Hydrocarbons/adverse effectsABSTRACT
OBJECTIVE: To investigate the association of exposure to polycyclic aromatic hydrocarbons exposure scores and alteration of relative mitochondrial DNA copy number of blood with female lung cancer risk among never smokers. METHODS: From August 2017 to August 2021, we enrolled all physician diagnosed new cases(n=465) of non-smoking female lung cancer from 12 tertiary and above hospitals in Liaoning, Jiangsu, Anhui and Qinghai provinces. And we selected matched non-smoking controls(n=463) by age and sex who were non-cancer and noncommunicable disease patients from the same hospital visited by the cases. Blood mitochondrial DNA copy number was detected by quantitative real-time polymerase chain reaction and estimated by relative quantification. We performed random forest and logistic regression to analyze the association of polycyclic aromatic hydrocarbons exposure scores and relative mitochondrial DNA copy number with the risk of female lung cancer among never smokers. We further analyzed the mediating effect and interaction models of polycyclic aromatic hydrocarbons exposure scores and mitochondrial DNA copy number levels on lung cancer in non-smoking women. RESULTS: The M(P25, P75) of polycyclic aromatic hydrocarbons exposure scores for cases and controls were 0.05(0.13, 0.16) and 0.08(0.24, 0.13), polycyclic aromatic hydrocarbons exposure scores of the cases was significantly higher than the controls(U=92130, P<0.05). The M(P25, P75) of mitochondrial DNA copy number for cases and controls were 0.90(0.71, 1.14) and 1.00(0.79, 1.21), mitochondrial DNA copy number of the cases was significantly lower than the controls(U=122559, P<0.05). Random forest and multivariable logistic regression analysis showed that the risk of lung cancer in non-smoking women increased with the increase of polycyclic aromatic hydrocarbons exposure scores(P_(trend)<0.05) and the decrease of relative mitochondrial DNA copy number(P_(trend)<0.05). The additive interaction between polycyclic aromatic hydrocarbons exposure scores and mitochondrial DNA copy number in non-smoking female lung cancer was statistically significant [API = 0.43(95%CI 0.19-0.67), SI = 2.84(95%CI 1.25-6.48). Mediation analysis showed mitochondrial DNA copy number had no significant mediating effect on the association between polycyclic aromatic hydrocarbons exposure scores and lung cancer in non-smoking women(Za×Zb: 95%CI-0.044-0.055). CONCLUSION: Minimize unnecessary polycyclic aromatic hydrocarbons exposures might significantly reduce the lung cancer risk among non-smoking women. Alteration of mitochondrial DNA copy number might become a potential biomarker in risk prediction of lung cancer of non-smoking women.
Subject(s)
Lung Neoplasms , Polycyclic Aromatic Hydrocarbons , Humans , Female , DNA, Mitochondrial/genetics , Polycyclic Aromatic Hydrocarbons/adverse effects , DNA Copy Number Variations , Smokers , Lung Neoplasms/geneticsABSTRACT
OBJECTIVES: Polycyclic aromatic hydrocarbons (PAHs) are environmental endocrine-disrupting compounds, which have been widely recognised as a risk factor for human health. However, the relationship between PAHs exposure and the risk of osteoarthritis has rarely been reported. This study aimed to investigate the association between individual and mixed exposure to PAHs and osteoarthritis. METHODS: In this cross-sectional study, participants aged ≥20 years with data on urinary PAHs and osteoarthritis were extracted from the National Health and Nutrition Examination Survey (NHANES) between 2001 and 2016. Logistic regression analysis was utilised to assess the relationship between individual PAHs exposure and osteoarthritis. The quantile-based g computation (qgcomp) analysis and Bayesian kernel machine regression (BKMR) analysis were performed to assess the effect of mixed exposure to PAHs on osteoarthritis, respectively. RESULTS: A total of 10,613 participants were enrolled, 980 (9.23%) of whom had osteoarthritis. Exposure to high levels of 1-hydroxynaphthalene (1-NAP) [odds ratio (OR)=1.06, 95% confidence interval (CI): 1.01-1.10], 3-hydroxyfluorene (3-FLU) (OR=1.09, 95%CI: 1.02-1.17), and 2-hydroxyfluorene (2-FLU) (OR=1.06, 95%CI: 1.01-1.13) were all associated with greater odds of osteoarthritis after adjusting for age, sex, body mass index, drinking alcohol, and hypertension. The qgcomp analysis showed that the joint weighted value of mixed PAHs exposure (OR=1.11, 95%CI: 1.02-1.22; p=0.017) was significantly related to higher odds of osteoarthritis. The BKMR analysis demonstrated that mixed exposure to PAHs was positively correlated with the risk of osteoarthritis. CONCLUSIONS: Both individual and mixed exposure to PAHs were positively correlated with the risk of osteoarthritis.
Subject(s)
Osteoarthritis , Polycyclic Aromatic Hydrocarbons , Adult , Humans , Polycyclic Aromatic Hydrocarbons/adverse effects , Nutrition Surveys , Cross-Sectional Studies , Bayes Theorem , Biomarkers , Osteoarthritis/chemically induced , Osteoarthritis/epidemiologyABSTRACT
BACKGROUND: Polycyclic aromatic hydrocarbons (PAHs) are environmental pollutants that are potentially hazardous to human health. Dietary exposure is recognized as one of the major pathways of exposure to PAHs among humans. While some PAH exposures have been associated with metabolic syndrome (MetS) in the general population, most epidemiological studies are based on urinary metabolites of a few noncarcinogenic PAHs. OBJECTIVE: To investigate the association between estimates of dietary exposure to major carcinogenic PAHs and MetS in Korean adults. METHODS: Multi-cycle Korean National Health and Nutrition Examination Survey (KNHANES) database (n = 16,015) and PAH measurement data from the total diet survey were employed to estimate daily PAH intake for each participating adult. After adjusting for potential confounders, multinomial logistic regression analysis was used to calculate the odds ratios (ORs) and 95% confidence intervals (CIs) between PAHs and MetS of the participating adults. RESULTS: Benzo(a)pyrene exposure was associated with an increased risk of MetS in men (OR = 1.30; 95% Cl: 1.03-1.63; P-trend = 0.03). In women, however, only chrysene and low high-density lipoprotein (HDL-c) were positively associated with an increased risk of MetS (OR = 1.24; 95% CI: 1.03-1.48; P-trend = 0.0172). Among men, smokers were at an increased risk for MetS, regardless of whether they were exposed to low or high total PAHs and benzo(a)pyrene levels. SIGNIFICANCE: Our findings suggested that PAHs are associated with the risk of MetS and MetS components in Korean adults. In particular, it was confirmed that smoking may influence the relationship between PAH exposure and MetS.Further prospective cohort studies are required to confirm the causal relationship between PAHs and MetS. IMPACT STATEMENT: Epidemiological studies on PAH exposure are often hampered by a lack of reliable exposure estimates, as biomonitoring of urine does not capture exposure to more toxic PAHs. Using multi-cycle KNHANES data and the measurement data from a total diet survey of Korea, we could develop a personalized PAH intake estimate for each participating adult and assessed the association with MetS.
Subject(s)
Metabolic Syndrome , Polycyclic Aromatic Hydrocarbons , Smoking , Adult , Female , Humans , Male , Benzo(a)pyrene/analysis , Biomarkers/urine , Dietary Exposure/analysis , Metabolic Syndrome/chemically induced , Metabolic Syndrome/epidemiology , Nutrition Surveys , Polycyclic Aromatic Hydrocarbons/adverse effects , Polycyclic Aromatic Hydrocarbons/analysis , Prevalence , Republic of Korea/epidemiology , Smoking/adverse effects , Smoking/epidemiologyABSTRACT
BACKGROUND: We previously showed that exposure to 5-methylchrysene (5MC) and other methylated polycyclic aromatic hydrocarbons (PAHs) best explains lung cancer risks in a case-control study among non-smoking women using smoky coal in China. Time-related factors (e.g., age at exposure) and non-linear relations were not explored. OBJECTIVE: We investigated the relation between coal-derived air pollutants and lung cancer mortality using data from a large retrospective cohort. METHODS: Participants were smoky (bituminous) or smokeless (anthracite) coal users from a cohort of 42,420 subjects from four communes in XuanWei. Follow-up was from 1976 to 2011, during which 4,827 deaths from lung-cancer occurred. Exposures were predicted for 43 different pollutants. Exposure clusters were identified using hierarchical clustering. Cox regression was used to estimate exposure-response relations for 5MC, while effect modification by age at exposure was investigated for cluster prototypes. A Bayesian penalized multi-pollutant model was fitted on a nested case-control sample, with more restricted models fitted to investigate non-linear exposure-response relations. RESULTS: We confirmed the strong exposure-response relation for 5MC (Hazard Ratio [95% Confidence Interval] = 2.5 [2.4, 2.6] per standard-deviation (SD)). We identified four pollutant clusters, with all but two PAHs in a single cluster. Exposure to PAHs in the large cluster was associated with a higher lung cancer mortality rate (HR [95%CI] = 2.4 [2.2, 2.6] per SD), while exposure accrued before 18 years of age appeared more important than adulthood exposures. Results from the multi-pollutant model identified anthanthrene (ANT) and benzo(a)chrysene (BaC) as risk factors. 5MC remained strongly associated with lung cancer in models that included ANT and BaC and also benzo(a)pyrene (BaP). CONCLUSION: We confirmed the link between PAH exposures and lung cancer in smoky coal users and found exposures before age 18 to be especially important. We found some evidence for the carcinogen 5MC and non-carcinogens ANT and BaC.
Subject(s)
Air Pollutants , Lung Neoplasms , Polycyclic Aromatic Hydrocarbons , Humans , Female , Adult , Adolescent , Polycyclic Aromatic Hydrocarbons/adverse effects , Polycyclic Aromatic Hydrocarbons/analysis , Case-Control Studies , Retrospective Studies , Coal/adverse effects , Coal/analysis , Life Change Events , Bayes Theorem , Air Pollutants/adverse effects , Lung Neoplasms/chemically induced , Carcinogens , China/epidemiologyABSTRACT
Exposure to fine particles (PM2.5) and associated PAHs are frequently linked with lung cancer, which makes the understanding of their occurrence and health risk in human lungs urgently important. Using the ultrasonic treatment and sequencing centrifugation (USC) extraction method coupled with gas chromatography-tandem mass spectrometry (GC - MS/MS) analysis, we revealed the molecular fingerprints of PM-accumulated PAHs in human lungs from a cohort of 68 patients with lung cancer in a typical air-polluted region, China. Sixteen priority PAHs can be grouped by concentrations as â¼ 1 × 104 ng/g (ANT/BkF/ACE/DBA/BgP/PHN/PYR), 2-5 × 103 ng/g (BaP/FLE/NaP/BbF), and â¼ 1 × 103 ng/g (IND/Acy/CHR/FLT/BaA). The sum concentration of 16 PAHs was approximately equaled to 13% of those in atmospheric PM2.5, suggesting significant pulmonary leaching of PAHs deposited in lungs. Low- and high-molecular weight PAHs accounted for â¼ 41.8% and â¼ 45.1% of the total PAHs, respectively, which indicated that atmospheric PM2.5, tobacco and cooking smoke were likely to be important sources of pulmonary PAHs. The evident increasing concentrations of NaP and FLE in pulmonary PM were significantly correlated with smoking history among smokers. The implicated carcinogenic potency of PM-accumulated PAHs among the participants aged 70-80 was 17 times that among participants aged 40-50 on the basis of BaP equivalent concentration (BaPeq) evaluation. The particulate enrichment factor (EFP), the PAH content in pulmonary PM relative to the bulk lung tissue, was equaled to 54 â¼ 835 and averaged at 436. The high value of EFP suggested that PAHs were essentially accumulated in pulmonary PM and exhibited a pattern of "hotspot" distribution in the lungs, which would likely increase the risk of monoclonal tumorigenesis. The chemical characteristics of PM-accumulated PAHs in human lungs together with their implicated lung cancer risks could provide significant information for understanding health effects of particulate pollution in the human body.
Subject(s)
Air Pollutants , Lung Neoplasms , Polycyclic Aromatic Hydrocarbons , Humans , Particulate Matter/adverse effects , Particulate Matter/analysis , Polycyclic Aromatic Hydrocarbons/adverse effects , Polycyclic Aromatic Hydrocarbons/analysis , Air Pollutants/adverse effects , Air Pollutants/analysis , Tandem Mass Spectrometry , Environmental Monitoring , Dust/analysis , Risk Assessment , Lung/chemistry , Lung Neoplasms/etiologyABSTRACT
OBJECTIVE: Recent studies have found that polycyclic aromatic hydrocarbons (PAHs) exposure may increase the risk of cardiovascular disease. The present study aimed to explore the association between PAHs exposure and severe abdominal aortic calcification (AAC) in adults. METHODS: Data were collected from the 2013-2014 National Health and Nutrition Examination Survey. PAHs exposure was analyzed from urinary mono hydroxylated metabolites of PAHs. Logistic regression models and subgroup analysis were performed to explore the association of PAHs exposure with severe AAC prevalence. RESULTS: A total of 1,005 eligible individuals were recruited into the study. After adjusting for confounding factors, those with the highest quartiles of 1-hydroxynaphthalene (1-NAP: OR 2.19, 95% CI 1.03-4.68, Pfor trend < 0.001), 2-hydroxynaphthalene (2-NAP: OR 2.22, 95% CI 1.04-4.64, Pfor trend < 0.001) and 1-hydroxypyrene (1-PYR: OR 2.15, 95% CI 1.06-4.33, Pfor trend < 0.001) were associated with an increased prevalence of severe AAC in the adults compared to those who in the lowest quartile. CONCLUSION: This study found that urinary 1-NAP, 2-NAP and 1-PYR were positively associated with severe AAC prevalence in adults.
Subject(s)
Polycyclic Aromatic Hydrocarbons , Humans , Adult , Polycyclic Aromatic Hydrocarbons/adverse effects , Polycyclic Aromatic Hydrocarbons/metabolism , Nutrition Surveys , Naphthalenesulfonates , BiomarkersABSTRACT
BACKGROUND: The primary aim of this study is to examine the association between urinary polycyclic aromatic hydrocarbons (PAHs) and diabetes mellitus (DM) among the US population. METHODS: We used data from the National Health and Nutritional Examination Survey 2003-16, which is a nationally representative population-based survey of the US non-institutionalized population. Logistic regression analysis was performed to evaluate the association between urinary PAHs and the prevalence of DM using odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: The study sample including 13 792 individuals ≥18 y of age. The average ages of the three PAH tertiles were 42.56±19.67, 42.21±19.51 and 43.39±17.99 y. An increased risk of DM was found with increased odds for the second (OR 1.56 [95% CI 1.36 to 1.79]) and third tertile (OR 1.79 [95% CI 1.55 to 2.06)] of urinary PAH as compared with the first tertile. Similarly, higher chances of DM were observed in the second (men: OR 1.42 [95% CI 1.18 to 1.71]; women: OR 1.76 [95% CI 1.44 to 2.14]) and third tertile (men: OR 1.69 [95% CI 1.38 to 2.08]; women: OR 1.79 [95% CI 1.46 to 2.19]) of urinary PAHs as compared with the first tertile in both men and women. CONCLUSIONS: A population-based cross-sectional study found a positive association between urinary PAHs and DM in the US population.
Subject(s)
Diabetes Mellitus , Polycyclic Aromatic Hydrocarbons , Male , Humans , Female , Polycyclic Aromatic Hydrocarbons/adverse effects , Polycyclic Aromatic Hydrocarbons/analysis , Polycyclic Aromatic Hydrocarbons/metabolism , Cross-Sectional Studies , Environmental Exposure/adverse effects , Nutrition Surveys , Biomarkers/urineABSTRACT
OBJECTIVE: To evaluate the interaction effects of Polycyclic aromatic hydrocarbons (PAHs) exposure and variants in cGAS-STING genes on mitochondrial DNA copy number (mtDNAcn) in workers. METHODS: The mtDNAcn was determined by real-time quantitative polymerase-chain reaction in 544 PAHs-exposed workers and 238 office workers. The polymorphisms were detected by flight mass spectrometry. RESULTS: The mtDNAcn in PAHs exposure group was significantly lower than non-occupational exposure population (P < 0.00). The cGAS rs610913 CA+AA had significant interaction effects with STING rs11554776 GG+GA (P = 0.035), rs7380824 CC+CT (P = 0.026), and rs78233829 GC+CC (P = 0.034) on mtDNAcn. The generalized linear model results showed that the influencing factors of mtDNAcn include PAHs exposure (P < 0.001) and the interaction of PAHs exposure and cGAS rs 311678 AA+AG (P = 0.047). CONCLUSION: The influencing factors of mtDNAcn include PAHs exposure and the interaction of PAHs exposure and cGAS rs 311678 AA+AG.
Subject(s)
Coke , Membrane Proteins , Nucleotidyltransferases , Polycyclic Aromatic Hydrocarbons , Humans , Coke/adverse effects , DNA Copy Number Variations , DNA, Mitochondrial/genetics , Nucleotidyltransferases/genetics , Polycyclic Aromatic Hydrocarbons/adverse effects , Membrane Proteins/genetics , Occupational Exposure/adverse effectsABSTRACT
Aim: To evaluate the association between urinary polycyclic aromatic hydrocarbon (PAH) metabolites and the risk of endometriosis. Methods: This cross-sectional study obtained data on women aged 20-54 years from the National Health and Nutrition Examination Survey (NHANES) 2001-2006. The weighted multivariate logistic regression model was established to assess the association between the eight urinary PAH metabolites and the risk of endometriosis. In this multivariate analysis, the eight urinary PAH metabolites were adjusted with urinary creatinine, and were divided into three groups according to tertiles: Tertile 1, Tertile 2 and Tertile 3. To evaluate the overall association of mixed PAH metabolites with endometriosis, the Bayesian kernel machine regression (BKMR) model was applied. Results: Totally 1,291 women were included, of which 90 (6.97%) had endometriosis and 1,201 (93.03%) did not have endometriosis. After adjusting for age, race, smoking, age at menarche, hysterectomy, ovary removed, female hormone use, and menopause, compared with the Tertile 1 group, the Tertile 2 and Tertile 3 groups of all PAH metabolites demonstrated no significant risk of endometriosis. A positive tendency was found between mixed PAH metabolites and endometriosis when all the metabolites were at their 60th percentile levels or above compared with their median levels. When all the other metabolites were fixed at their median levels, 1-hydroxynaphthalene was positively correlated with endometriosis. Potential interactions existed between 1-hydroxynaphthalene and 2-hydroxynaphthalene and between 2-hydroxyfluorene and 3-hydroxyfluorene. Conclusion: No significant association was found between individual PAH metabolites and endometriosis. A positive association existed between mixed PAH metabolites and the risk of endometriosis.