Polycyclic Aromatic Hydrocarbons (PAHs) and Their Importance in Animal Nutrition

Polycyclic aromatic hydrocarbons (PAHs) formed as a result of incomplete combustion of organic compounds. It contains compounds that cause toxic, teratogenic, mutagenic and carcinogenic damage, such as heterocyclic aromatic amines, benzene and formaldehyde. PAHs can be found in industrial wastes, garbage, cigarette smoke, pesticides and flue gases and can contaminate air, water, soil and food. Although more than 100 PAH compounds are detected in nature, it is accepted that 16 PAH compounds have more harmful effects. It is important to determine the PAH exposure levels of feeds used in animal nutrition, since the contamination of feed plants and factory feeds with PAH compounds will indirectly affect human health. In this study, the physical and chemical properties of PAHs and their effects on animal production and indirectly on human health were compiled.

Relationship Between Polycyclic Aromatic Hydrocarbons and Cardiovascular Diseases: A Systematic Review

Objective: The primary aim of this systematic review was to examine the relationship of polycyclic aromatic hydrocarbon (PAH) exposure with cardiovascular diseases (CVDs) and elaborate the current knowledge and recent advances in the area of PAH and its effects on CVDs and discuss the growing epidemiological evidence linking PAH to CVDs on the health of human populations. In this systematic review, the increased risk of cardiovascular diseases and their relationship with PAHs were discussed in detail.Methods: On 05th April 2021, a systematic literature search was conducted using PubMed/Medline and Web of Science search engines in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) criteria. The search was limited to articles that were written in English and dealt with human issues. All original peer-review publications were considered for inclusion. Comments, case reports, reviews, duplicated papers, and conference reports were excluded. Data was collected from included papers by two independent reviewers.Results: Conclusively, 20 research articles published between 2005 and 2021 were chosen for the final analysis. The systemic review included 20 studies with a variety of geographical studies. The most common research category among the nominated studies were time-series studies followed by retrospective cohort, cross-sectional, quasi-experimental, panel, and case-control studies. Most of the studies were conducted in the United States, whereas others were showed in various geographical countries around the world, such as Denmark, Germany, Finland, Netherlands, France, China, Norway, Korea, Sweden, Saudi Arabia, and Belgium. Eight studies assessed the association between PAH exposure and CVDs, four articles observed this relationship with blood pressure (BP), two observed association between atherosclerotic CVD and PAH, one congenital heart disease, cardiovascular events, and two with obesity. Furthermore, in some investigations, a favorable association between PAH exposure and hypertension as well as PAH exposure and obesity was found.Conclusion: In conclusion, this systematic review examined the relationship of PAH exposure with CVDs and CVD-related risk factors by searching several digital databases. After a comprehensive literature searches and summarizing findings from 20 articles, the authors concluded that a positive relationship was observed between PAH exposure and CVD risks.

PIG-A gene mutation as a genotoxicity biomaker in polycyclic aromatic hydrocarbon-exposed barbecue workers

Background The PIG-A gene mutation assay is a valuable tool for measuring in vivo gene mutations in blood cells. The human PIG-A assay, used as a potential genotoxicity biomarker, is minimally invasive, sensitive, and cost-efficient; however, the relationship between carcinogen exposure and PIG-A mutations is not well understood. Methods We investigated the genotoxic effect of red blood cells using PIG-A assay and lymphocyte cytokinesis-block micronucleus test in barbecue restaurant workers (N = 70) exposed to polycyclic aromatic hydrocarbons (PAHs) and self-identified healthy control subjects (N = 56). Urinary PAH metabolites were measured to evaluate internal exposure levels. Results Multivariate Poisson regression showed that the PAH-exposed workers exhibited significantly higher PIG-A mutant frequency (MF) (8.04 ± 6.81 × 10− 6) than did the controls (5.56 ± 5.26 × 10− 6) (RR = 0.707, 95% CI: 0.615–0.812, P < 0.001). These results indicate that PAH exposure is a risk factor for elevated PIG-A MF. The frequencies of micronuclei (MN) and nuclear buds (NBUD) in the PAH-exposed workers (MN: 3.06 ± 2.07 ‰, NBUD: 1.38 ± 1.02 ‰) were also significantly higher than in the controls (MN: 1.46 ± 0.64 ‰, P < 0.001; NBUD: 0.70 ± 0.60 ‰, P < 0.001). Additionally, PIG-A MFs showed better associations with several urinary hydroxylated PAH metabolites (P2-OH-Flu = 0.032, r2-OH-Flu = 0. 268; P2-OH-Phe = 0.022, r2-OH-Phe = 0.286; P3-OH-Phe = 0.0312, r3-OH-Phe = 0.270; P4-OH-Phe = 0.018, r4-OH-Phe = 0.296), while the increase in MN, NPB, and NBUD frequencies was not associated with any OH-PAH metabolites; and high-PAH-exposed workers showed the highest PIG-A MFs. Furthermore, there was a significant association between PIG-A MF and PAH exposure levels (Chi-square test for trend, P = 0.006). Conclusions Our results indicate that an increase in PIG-A MF in barbecue workers could reflect the response to PAH exposure, providing evidence of its potential as a genotoxicity biomarker in human risk assessment.

Effects of environmental polycyclic aromatic hydrocarbon exposure and pro-Inflammatory activity on Type 2 Diabetes Mellitus

ABSTRACTBackgroundPolycyclic aromatic hydrocarbons (PAHs) are formed due to incomplete combustion and known for their potential impact and persistence in the environment. PAHs exposure have been linked to cause adverse health effect including cancer and genetic mutations. The understanding of metabolic effects of PAH exposure are still less clear especially in the presence of pro-inflammatory stress like alcoholism or diabetes.ObjectiveThe aim of this article is to understand the metabolic effects of PAH exposure by analyzing the clinical biomarkers. This study has also accessed the interactive impact of PAH and other proinflammatory factors, like alcohol intake on the metabolic syndrome, especially Type 2 Diabetes Mellitus (T2DM).MethodsAll the data in this study are retrieved from CDC NHANES (2015-16). We investigated urinary levels of hydroxylated PAH metabolites (OH-PAHs) along with demographic, clinical and laboratory data. Questionnaire data for alcohol use and diabetes status were also included along with laboratory data. Laboratory measures included in the study were levels of PAHs, glycohemoglobin, glucose, cholesterol, lipids, triglyceride, complete blood count, lymphocytes, and monocytes. Generalize linear model Univariate factorial ANOVA was used to evaluate the group differences (both between the groups; as well as across all the groups) 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.ResultsBMI (p=0.002), and age (≤0.001) are independent demographic risk factors for T2DM in high PAH exposure. Acute proinflammatory activity characterized by CRP, is augmented by elevated monocyte levels (p≤0.001) and stepwise addition of 1-HN (p=0.005), and 2-HN (p=0.001) independently. Prevalence of highest average drinks over time is observed in the high PAH exposure; with males drinking almost twice compared to females in Gr.3. 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 PAH exposure.DiscussionIn this large dataset investigation on humans, the adverse effects of high exposure of PAHs identified candidate demographic risk factors. Preclinical experimental studies on mice have suggested that PAHs exposure induces lipid metabolic disorders in a time-dependent manner, which we found in humans too. Sexual dimorphism is observed in alcohol drinking with males drinking more in the high PAH exposure group. Alcohol drinking as an independent factor associated with the DMT2 indicator, HbA1C in individuals with high PAH exposure.HighlightsBMI and Age are demographic risk factors for Diabetes Mellitus Type 2 (DMT2) in high PAH exposureAcute proinflammatory activity characterized by CRP, is augmented by elevated monocyte levels and 1-HN and 2-HN independentlyPrevalence of higher average drinks over time is observed with high PAH exposurePathway of DMT2 shows sexual dimorphism, with males showing association with triglycerides, and females with CRP independently with HbA1CThe arrangement of CRP, absolute monocyte levels, serum triglycerides and average drinks over time predict the HbA1C levels in individuals with high PAH exposure.

Looking For Polycyclic Aromatic Hydrocarbon Metabolizing Microorganisms In The Oral Cavity of Smokers

Certain soil microbes resist and metabolize polycyclic aromatic hydrocarbons (PAHs). The same is true for certain skin microbes. Oral microbes have the potential to oxidize tobacco PAHs to increase their ability to cause cancer. We hypothesized that oral microbes that resist high levels of PAH in smokers exist and can be identified based on their resistance to PAHs. We isolated bacteria and fungi that survived long term in minimal media with PAHs as the sole carbon source from the oral cavity in 11 of 14 smokers and only 1 of 6 nonsmokers. Of bacteria genera that included species that survived harsh PAH exposure in vitro, all were found at trace levels on the oral mucosa, except for Staphylococcus and Actinomyces. Two PAH-resistant strains of Candida albicans (C. albicans) were isolated from smokers. C. albicans is found orally at high levels in tobacco users and some Candida species can metabolize PAHs. The two C. albicans strains were tested for metabolism of two model PAH substrates, pyrene and phenanthrene. The result showed that the PAH-resistant C. albicans strains did not metabolize the two PAHs. In conclusion, evidence for large scale oral microbial metabolism of tobacco PAHs by common oral microbes remains lacking.

Multi-Media Exposure to Polycyclic Aromatic Hydrocarbons at Lake Chaohu, the Fifth Largest Fresh Water Lake in China: Residual Levels, Sources and Carcinogenic Risk

The residual levels of 16 priority polycyclic aromatic hydrocarbons (PAHs) in environment media and freshwater fish were collected and measured from Lake Chaohu by using Gas chromatography-mass spectrometry. Potential atmospheric sources were identified by molecular diagnostic ratios and the positive matrix factorization (PMF) method. PAH exposure doses through inhalation, intake of water and freshwater fish ingestion were estimated by the assessment model recommended by US EPA. The carcinogenic risks of PAH exposure were evaluated by probabilistic risk assessment and Monte Carlo simulation. The following results were obtained: (1) The PAH16 levels in gaseous, particulate phase, water and fish muscles were 59.4 ng·m−3, 14.2 ng·m−3, 170 ng·L−1 and 114 ng·g−1, respectively. No significant urban-rural difference was found between two sampling sites except gaseous BaPeq. The relationship between gaseous PAHs and PAH in water was detected by the application of Spearman correlation analysis. (2) Three potential sources were identified by the PMF model. The sources from biomass combustions, coal combustion and vehicle emission accounted for 43.6%, 30.6% and 25.8% of the total PAHs, respectively. (3) Fish intake has the highest lifetime average daily dose (LADD) of 3.01 × 10−6 mg·kg−1·d−1, followed by the particle inhalation with LADD of 2.94 × 10−6 mg·kg−1·d−1. (4) As a result of probabilistic cancer risk assessment, the median ILCRs were 3.1 × 10−5 to 3.3 × 10−5 in urban and rural residents, which were lower than the suggested serious level but higher than the acceptable level. In summary, the result suggests that potential carcinogenic risk exists among residents around Lake Chaohu. Fish ingestion and inhalation are two major PAH exposure pathways.

Impact of Polycyclic Aromatic Hydrocarbon Accumulation on Oyster Health

In the past decade, the Deepwater Horizon oil spill triggered a spike in investigatory effort on the effects of crude oil chemicals, most notably polycyclic aromatic hydrocarbons (PAHs), on marine organisms and ecosystems. Oysters, susceptible to both waterborne and sediment-bound contaminants due to their filter-feeding and sessile nature, have become of great interest among scientists as both a bioindicator and model organism for research on environmental stressors. It has been shown in many parts of the world that PAHs readily bioaccumulate in the soft tissues of oysters. Subsequent experiments have highlighted the negative effects associated with exposure to PAHs including the upregulation of antioxidant and detoxifying gene transcripts and enzyme activities such as Superoxide dismutase, Cytochrome P450 enzymes, and Glutathione S-transferase, reduction in DNA integrity, increased infection prevalence, and reduced and abnormal larval growth. Much of these effects could be attributed to either oxidative damage, or a reallocation of energy away from critical biological processes such as reproduction and calcification toward health maintenance. Additional abiotic stressors including increased temperature, reduced salinity, and reduced pH may change how the oyster responds to environmental contaminants and may compound the negative effects of PAH exposure. The negative effects of acidification and longer-term salinity changes appear to add onto that of PAH toxicity, while shorter-term salinity changes may induce mechanisms that reduce PAH exposure. Elevated temperatures, on the other hand, cause such large physiological effects on their own that additional PAH exposure either fails to cause any significant effects or that the effects have little discernable pattern. In this review, the oyster is recognized as a model organism for the study of negative anthropogenic impacts on the environment, and the effects of various environmental stressors on the oyster model are compared, while synergistic effects of these stressors to PAH exposure are considered. Lastly, the understudied effects of PAH photo-toxicity on oysters reveals drastic increases to the toxicity of PAHs via photooxidation and the formation of quinones. The consequences of the interaction between local and global environmental stressors thus provide a glimpse into the differential response to anthropogenic impacts across regions of the world.

A High Concentration of Polycyclic Aromatic Hydrocarbons in Umbilical Cord Tissue is Associated with An Increased Risk For Fetal Neural Tube Defects

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous in the environment and have detrimental effects on human health. Embryos are particularly susceptible to environmental insults such as PAHs. We examined the association between prenatal exposure to PAHs and the risk for fetal neural tube defects (NTDs). A case-control study was conducted with 119 NTD cases and 119 controls. A total of 16 PAHs in umbilical cord tissue, determined with gas chromatography–mass spectrometry, were used as in utero exposure markers. Logistic regression and Bayesian kernel machine regression (BKMR) were performed to evaluate the individual and overall effects of PAH exposure on the risk for NTDs, respectively. Median concentrations of 10 PAHs were significantly higher in cases than in controls. In logistic regression, concentrations of four PAHs above the median of all participants were significantly associated with an increased NTD risk, even when potential covariates were adjusted for: phenanthrene, 2.35-fold (95% confidence interval [CI] 1.04–5.34); fluoranthene, 2.37-fold (95% CI 1.02–5.48); pyrene, 2.41-fold (95% CI 1.04–5.62); and benzo(b)fluoranthene, 2.95-fold (95% CI 1.27–6.86). In BKMR, the risk for NTDs increased when PAH concentrations were all above their 65th percentile compared to their median, while no statistical association between a single compound and NTD risk was observed when the remaining nine PAHs were taken into consideration simultaneously. Together these results show that prenatal PAH exposure is a risk factor for NTDs in offspring.

Association between Polycyclic Aromatic Hydrocarbon Exposure and Diarrhea in Adults

Objective: Polycyclic aromatic hydrocarbons (PAHs) are not only natural but also anthropogenic contaminants that exist in many places in the environment. Human beings often accidentally ingest PAHs via smoking. Furthermore, smoking may increase the risk of bowel disorder, including diarrhea and other gastrointestinal problems. Therefore, PAH exposure is hypothesized to be related to diarrhea risk. This study discusses the association between diarrhea and PAH exposure in the United States adult population. Method: 10,537 participants from the National Health and Nutrition Examination Survey (NHANES 2001–2006) were involved in this cross-sectional analysis. Bowel disorders were assessed via examination of stool frequency and stool type. The concentrations of urinary PAH metabolites were used to evaluate PAH exposure. The association between bowel habits and PAH exposure was assessed using a multivariate logistic regression model with covariate assessment of gender, age, race, liver function, kidney function, and common chronic health diseases. Results: All PAH metabolites except 1-hydroxynaphthalene, 1-hydroxypyrene, and 9-hydroxyfluorene were substantially correlated with an increased risk of diarrhea (p < 0.05) after modification of relevant covariables. This study also revealed significant association in the group of females (p < 0.05). Furthermore, all PAH metabolites except 1-hydroxynaphthalene, 2-hydroxyphenanthrene, 1-hydroxypyrene, and 9-hydroxyfluorene show significantly positive association in the non-obesity group (BMI < 30, p < 0.05). Conclusions: PAH exposure is highly associated with risk of bowel disorders among the adult population in the United States, especially in female and non-obesity populations. More research is necessary to shed light on the pathophysiological mechanisms associated to PAH exposure and diarrhea.