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Polycyclic aromatic hydrocarbons (PAHs), one of the major environmental pollutants, produced from incomplete combustion of materials like coal, oil, gas, wood, and charbroiled meat, that contaminate the air, soil, and water, necessitating urgent remediation. Understanding the metabolic pathways for PAHs degradation is crucial to preventing environmental damage and health issues. Biological methods are gaining increasing interest due to their cost-effectiveness and environmental friendliness. These methods are particularly suitable for remediating PAHs contamination and mitigating associated risks. The paper also outlines the processes for biodegrading PAHs, emphasizing the function of Pseudomonas spp., a kind of bacterium recognized for its capacity to degrade PAHs. To eliminate PAHs from the environment and reduce threats to human health and the environment, Pseudomonas spp. is essential. Understanding the mechanism of PAH breakdown by means of microbes could lead to effective clean-up strategies. The review highlights the enzymatic capabilities, adaptability, and genetic versatility of the genes like nah and phn of Pseudomonas spp., which are involved in PAHs degradation pathways. Scientific evidence supports using Pseudomonas spp. as biocatalysts for PAHs clean-up, offering cost-effective and eco-friendly solutions.

Exposure to polycyclic aromatic hydrocarbons (PAH), generated through incomplete combustion of organic materials such as coal and wood, and through activities, like charbroiling meat and smoking tobacco, negatively impact children's health. This study evaluates early-life PAH exposure in children from Southern India and its association with early childhood caries (ECC). We utilized maternal and child urine samples from the Household Air Pollution Intervention Network (HAPIN) cohort to measure PAH metabolites: 2-naphthol (2-NAP) and 1-hydroxypyrene (1-PYR). We evaluated presence of dental caries in children (n = 712) using decayed, missing, and filled surfaces (dmfs) index. Socio-demographic data and dietary recall information were collected through questionnaires. Data analysis was conducted using a negative binomial hurdle model. Dental caries prevalence was high, with 53.6 % of participants having cavitated lesions, 13.6 % showing non-cavitated lesions, and 32.8 % classified as caries-free. Elevated urinary concentrations of 2-NAP during first and third trimesters were associated with a 1.09-fold increase in caries incidence (95 % CI, 1.03-1.16 and 1.02-1.17, respectively). Postnatal exposure to 1-PYR at six months corresponded to an 8 % increase in ECC risk per log-unit rise (IRR, 1.08; 95 % CI, 1.02-1.16). Average postnatal PAH exposure (mean 96.55 μg/g creatinine) demonstrated a stronger link with each log-unit increase corresponding to an incident rate ratio (IRR) of 1.22 (95 % CI, 1.10-1.36) in the count model and an odds ratio (OR) of 1.36 (95 % CI, 1.06-1.63) in zero model. Categorical analyses revealed monotonic dose-response relationships, with children in the highest quartile of postnatal 2-NAP and 1-PYR exposure exhibiting 39 % and 35 % greater ECC burden, respectively, compared to those in the lowest quartile. Our findings suggest an association between PAH exposure and ECC, particularly during the first and third trimesters with lifestyle factors playing a modifying role. The compounded impact of co-exposure to smoke from secondhand smoke and biomass-based cooking underscores critical need to reduce PAH exposure during early childhood.

Polycyclic aromatic hydrocarbons (PAHs), including the Group 1 human carcinogen benzo[a]pyrene (BaP), are produced by the incomplete combustion of organic matter and thus are present in tobacco smoke, charbroiled food and diesel exhaust. The nematode Caenorhabditis elegans is an established model organism, however it lacks the genetic components of the classical mammalian cytochrome P450 (CYP)-mediated BaP-diol-epoxide metabolism pathway. We therefore introduced human CYP1A1 or CYP1A2 together with human epoxide hydrolase (EPHX) into the worm genome by Mos1-mediated Single Copy Insertion (MosSCI) and evaluated their response to BaP exposure via toxicological endpoints. Compared to wild-type control, CYP-humanised worms were characterised by an increase in pharyngeal pumping rate and a decrease in volumetric surface area. Furthermore, BaP exposure reduced reproductive performance, as reflected in smaller brood size, which coincided with the downregulation of the nematode-specific major sperm protein as determined by transcriptomics (RNAseq). BaP-mediated reproductive toxicity was exacerbated in CYP-humanised worms at higher exposure levels. Collagen-related genes were downregulated in BaP-exposed animals, which correlate with the reduction in volumetric size. Whole genome DNA sequencing revealed a higher frequency of T > G (A > C) base substitution mutations in worms expressing human CYP1A1;EPHX which aligned with an increase in DNA adducts identified via an ELISA method (but not classical 32P-postlabelling). Overall, the CYP-humanised worms provided new insights into the value of genome-optimised invertebrate models by identifying the benefits and limitations within the context of the (3Rs) concept which aims to replace, reduce and refine the use of animals in research.

Gastric cancer (GC) ranks third in terms of cancer-related deaths and is the fifth most commonly diagnosed type of cancer. Its risk factors include Helicobacter pylori infection, Epstein-Barr virus infection, the consumption of broiled and charbroiled animal meats, salt-preserved and smoke-enhanced foods, alcohol drinking, tobacco smoking, exposure to ionizing radiation, and positive family history. The limited effectiveness of conventional therapies and the widespread risk factors of GC encourage the search for new methods of treatment and prevention. In the quest for cheap and commonly available medications, numerous studies focus on herbal medicine, traditional brews, and spices. In this review, we outline the potential use of spices, including turmeric, ginger, garlic, black cumin, chili pepper, saffron, black pepper, rosemary, galangal, coriander, wasabi, cinnamon, oregano, cardamom, fenugreek, caraway, clove, dill, thyme, Piper sarmentosum, basil, as well as the compounds they contain, in the prevention and treatment of GC. We present the potential molecular mechanisms responsible for the effectivity of a given seasoning substance and their impact on GC cells. We discuss their potential effects on proliferation, apoptosis, and migration. For most of the spices discussed, we also outline the unavailability and side effects of their use.

Air quality degradation events in the urban environment are often attributed to anthropogenic aerosol sources related to combustion of liquid or solid fuels in various activities. The effects of massive cooking emissions during Greek nationwide traditional festivities were investigated by a combined characterization of particulate matter (PM) levels and organic aerosol (OA) sources. Focus was centered on periods around two major festivities, namely "Fat Thursday" and Easter Sunday along six different years. OA sources were apportioned through Positive Matrix Factorization (PMF) on Aerosol Chemical Speciation Monitor (ACSM) mass spectra, while the spatial characteristics of the episodes were assessed through a low-cost, sensor-based PM2.5 monitoring network operating in Athens and other Greek cities. Contrasts were examined by considering a 15-day period around each event, while the effect of the 2020-2021 mobility restrictions, related to COVID-19, was also assessed. An episode-specific cooking organic aerosol (COA) spectral profile was delineated, and can be considered as a reference for ambient COA from meat grilling. Severe pollution episodes that affected the entire Athens basin were recorded, with PM2.5 concentrations exceeding 300 μg m-3 on occasions. COA contributions dominated primary organic aerosol (POA) and made up almost half of OA concentrations. During "Fat Thursday" COA concentrations and contributions peaked during night-time (23.2 μg m-3 and 46 %, respectively) while for Easter Sunday COA maxima were recorded in the early afternoon (27.4 μg m-3 and 39 %). Analyzing a full-year OA source dataset, revealed a pronounced recreational cooking pattern in central Athens, with COA concentrations rising towards the weekend, reflecting the impact of the food service sector. In view of the upcoming review of the EU air quality directive, foreseeing stricter annual PM2.5 limits as well as 24-h limit values and related alerts, the mitigation of cooking emissions appears as a potent instrument for achieving tangible air quality benefits.

Glycidyl fatty acid esters (GEs) can be found in food, and they can be converted into genotoxic animal carcinogen glycidol in vivo by the action of lipase. This study examined whether human ingestion of charbroiled pork containing high levels of GEs (300 µg/day) increased glycidol-hemoglobin adduct (diHOPrVal), a marker of internal exposure to glycidol using LC-MS/MS. Contrary to expectation, the diHOPrVal value before ingesting charbroiled pork was 3.11 ± 1.10 pmol/g globin, which slightly decreased to 2.48 ± 0.47 pmol/g globin after 5 days of consumption. The decrease in lipase activity caused by the continuous consumption of lipid-rich foods such as meat in humans might decrease internal exposure to glycidol released from its esters. Thus, lipase activity was measured in C57/BL6J mice fed a high-fat diet (HFD) for 8 weeks, and diHOPrVal formation was measured after the administration of glycidyl oleate. Lipase activity was significantly lower in the HFD group than in the normal diet group. The amount of diHOPrVal was reduced in the HFD group. Therefore, the lipase activity was reduced by HFD, thereby decreasing the degradation of glycidol from glycidyl oleate. These results indicate that changes in lipase activity depending on the amount of lipids in the diet may affect the assessment of GEs exposure, and monitoring the lipase activity would provide a comprehensive understanding of exposure assessment.

Benzo(a)pyrene (BaP) is a polycyclic aromatic hydrocarbon and a serious environmental pollutant. BaP is formed by the incomplete combustion of organic matter at high temperatures. In addition, tobacco smoke and many foods, especially charbroiled food and grilled meats, contain BaP and can cause it to enter human body. Melatonin, a pineal gland hormone, has antioxidant, anti-apoptosis, and autophagy regulatory properties. The possible protective impact of melatonin on cardiopulmonary toxicity induced by BaP was investigated by examining the antioxidant effects and the apoptosis and autophagy properties of melatonin. Thirty male mice were divided into 5 groups and treated for 28 days as follows: (I) control (BaP and melatonin solvent), (II) BaP (75 mg/kg, oral gavage), (III and IV) BaP (75 mg/kg) + melatonin (10 and 20 mg/kg, intraperitoneally), (V) melatonin (20 mg/kg). The oxidative stress factors (MDA and GSH content) were assessed in the heart and lung tissues. The levels of apoptotic (Caspase-3 and the Bax/Bcl-2 ratio) and autophagic (the LC3 ӀӀ/Ӏ, Beclin-1, and Sirt1) proteins were examined by using western blot analysis. Following the administration of BaP, MDA, the Bax/Bcl-2 ratio, and the Caspase-3 proteins increased in the heart and lung tissues, while GSH, Sirt1, Beclin-1, and the LC3 II/I ratio diminished. The coadministration of melatonin along with BaP, MDA, and apoptotic proteins returned to the control values, while GSH and the autophagy proteins were enhanced in both the heart and lungs. Melatonin exhibited a protective effect against BaP-induced heart and lung injury through the suppression of oxidative stress and apoptosis and the induction of the Sirt1/autophagy pathway.

Previous investigations suggest that dietary sources of polycyclic aromatic hydrocarbons (PAHs) contribute to the PAH-DNA adduct load in peripheral white blood cells (WBCs). In the current study, we measured PAH-DNA adducts by enzyme-linked immunosorbent assay in WBCs obtained from 47 California wildland (forest) firefighters at two time points (early and late) during an active forest fire season. PAH-DNA adduct levels were not associated with recent firefighting activity, but were positively associated with frequency of charbroiled food consumption in the previous 2 weeks. In addition, adduct levels declined with time since last ingestion of charbroiled food. These studies indicate that recent consumption of charbroiled food contributes to the PAH-DNA adduct load in peripheral WBCs.

Carcinogenic polycyclic aromatic hydrocarbons (PAHs) form DNA adducts via a complex metabolic activation pathway that includes cytochrome P450 (CYP) 1A1, whereas intermediate metabolites can be detoxified by conjugation through pathways including glutathione s-transferase M1 (GSTM1). PAH-DNA adducts can be measured in peripheral white blood cells (WBCs) and should reflect the net effect of competing activation and detoxification pathways and DNA repair as well as exposure. We have previously shown that WBC PAH-DNA adducts measured by an enzyme-linked immunosorbent assay (ELISA) were associated with recent, frequent consumption of charbroiled food among 47 nonsmoking wildland fire-fighters who provided two blood samples 8 wk apart. In the investigation reported here, which was performed in the same population, we measured the association between the GSTM1 null genotype, which results in loss of enzyme activity, and PAH-DNA adduct levels, hypothesizing that subjects with this genotype would have higher levels of DNA adducts because of their decreased ability to detoxify PAH metabolites. However, PAH-DNA adduct levels were nonsignificantly lower in subjects with the GSTM1 null genotype (n = 28) compared with other subjects (n = 19) (median 0.04 fmol/microgram DNA vs 0.07 fmol/microgram DNA, respectively, P = 0.45, Wilcoxon rank-sum test). Adduct levels were also lower in the nine subjects heterozygous or homozygous for the CYP1A1 exon 7 polymorphism (which codes for a valine rather than isoleucine and is thought to be associated with greater CYP1A1 activity) compared with the 38 wild-type subjects (P = 0.12). In the entire group, there was a positive association between consuming charbroiled food and PAH-DNA adduct formation (r = 0.24, P = 0.02, Spearman rank-order correlation). This association was weaker in the subgroup of subjects with the GSTM1 null genotype (r = 0.03, P = 0.84) and stronger among the remaining subjects (r = 0.57, P = 0.0002). These results suggest that the GSTM1 null genotype and CYP1A1 exon 7 polymorphism are not associated with increased susceptibility for PAH-DNA adduct formation in peripheral WBCs measured by ELISA in nonsmoking populations.

Wildland (forest) firefighters are exposed to a wide range of carcinogenic polycyclic aromatic hydrocarbons (PAH) in forest fire smoke. PAH undergo metabolic activation and can subsequently bind to DNA. In this study, we investigated the association between occupational and dietary PAH exposures and the formation of WBC PAH-DNA adducts in a population of wildland firefighters. An enzyme-linked immunosorbent assay using an antiserum elicited against benzo(a)pyrene-modified DNA was used to measure PAH-DNA adducts in WBC obtained from 47 California firefighters at two time points, early and late in the 1988 forest fire season. PAH-DNA adduct levels were not associated with cumulative hours of recent firefighting activity. However, firefighters who consumed charbroiled food within the previous week had elevated PAH-DNA adduct levels, which were related to frequency of charbroiled food intake. These findings suggest that dietary sources of PAH contribute to PAH-DNA adduct levels in peripheral WBC and should be evaluated when using this assay to assess occupational and environmental PAH exposure.

Consumption of charbroiled red meat and meat-derived polycyclic aromatic hydrocarbons (PAHs) has been associated with risk of colorectal adenoma, a precursor of colorectal cancer. Furthermore, leukocyte PAH-DNA adduct levels have been demonstrated to increase in response to charbroiled red meat intake but to date there have been no studies that have investigated the relationship between leukocyte PAH-DNA adduct levels and risk of colorectal adenoma. We investigated the relation of leukocyte PAH-DNA adduct formation and colorectal adenoma in a clinic-based case-control study of colorectal adenomas. The study comprised 82 cases of colorectal adenoma and 111 polyp-free controls, none of whom were current smokers. Leukocyte PAH-DNA adducts were measured by a sensitive chemiluminescence immunoassay using an antiserum elicited against DNA modified with (+/-)-7beta,8alpha-dihydroxy-9alpha,10alpha-epoxy-7,8,9,10-tetrahydro-benzo[a]pyrene that recognizes several PAHs bound to human DNA. Leukocyte PAH-DNA adduct levels were higher among colorectal adenoma cases (median, 1.4 adducts per 10(8) nucleotides) than polyp-free controls (median, 1.2 adducts per 10(8) nucleotides) (P = 0.02). There was a positive association between PAH-DNA adduct level and adenoma prevalence: each unit increase in PAH-DNA adduct level (per 10(8) nucleotides) was associated with an odds ratio (OR) of 1.5 [95% confidence interval (CI), 1.1-2.2]. In addition, a comparison of the lowest quartile for PAH-DNA adduct level with the highest quartile yielded an OR of 2.8 (95% CI, 1.2-6.5; P(trend) = 0.048) for risk of colorectal adenoma. These data support a link between PAH exposure and colorectal adenoma.

Quantitation of DNA adducts in human tissues has been achieved with highly sensitive techniques based on adduct radiolabeling, antisera specific for DNA adducts or modified DNA, and/or adduct structural characterization using chemical instrumentation. Combinations of these approaches now promise to elucidate specific adduct structures and provide detection limits in the range of 1 adduct/10(9) nucleotides. Documentation of human exposure and biologically effective dose (i.e., chemical bound to DNA) has been achieved for a wide variety of chemical carcinogens, including polycyclic aromatic hydrocarbons (PAHs), aromatic amines, heterocyclic amines, aflatoxins, nitrosamines, cancer chemotherapeutic agents, styrene, and malondialdehyde. Due to difficulties in exposure documentation, dosimetry has not been precise with most environmental and occupational exposures, even though increases in human blood cell DNA adduct levels may correlate approximately with dose. Perhaps more significant are observations that lowering exposure results in decreasing DNA adduct levels. DNA adduct dosimetry for environmental agents has been achieved with dietary contaminants. For example, blood cell polycyclic aromatic hydrocarbon-DNA adduct levels were shown to correlate with frequency of charbroiled meat consumption in California firefighters. In addition, in China urinary excretion of the aflatoxin B1-N7-guanine (AFB1-N7-G) adduct was shown to increase linearly with the aflatoxin content of ingested food. Assessment of DNA adduct formation as an indicator of human cancer risk requires a prospective nested case-control study design. This has been achieved in one investigation of hepatocellular carcinoma and urinary aflatoxin adducts using subjects followed by a Shanghai liver cancer registry. Individuals who excreted the AFB1-N7-G adduct had a 9.1-fold adjusted increased relative risk of hepatocellular carcinoma compared to individuals with no adducts. Future advances in this field will be dependent on chemical characterization of specific DNA adducts formed in human tissues, more-precise molecular dosimetry, efforts to correlate DNA adducts with cancer risk, and elucidation of opportunities to reduce human DNA adduct levels.

Human cytochrome P450 enzymes involved in the bioactivation of estragole to its proximate carcinogen 1'-hydroxyestragole were identified and compared to the enzymes of importance for 1'-hydroxylation of the related alkenylbenzenes methyleugenol and safrole. Incubations with Supersomes revealed that all enzymes tested, except P450 2C8, are intrinsically able to 1'-hydroxylate estragole. Experiments with Gentest microsomes, expressing P450 enzymes to roughly average liver levels, indicated that P450 1A2, 2A6, 2C19, 2D6, and 2E1 might contribute to estragole 1'-hydroxylation in the human liver. Especially P450 1A2 is an important enzyme based on the correlation between P450 1A2 activity and estragole 1'-hydroxylation in human liver microsomal samples and inhibition of estragole 1'-hydroxylation by the P450 1A2 inhibitor alpha-naphthoflavone. Kinetic studies revealed that, at physiologically relevant concentrations of estragole, P450 1A2 and 2A6 are the most important enzymes for bioactivation in the human liver showing enzyme efficiencies (kcat/Km) of, respectively, 59 and 341 min-1 mM-1. Only at relatively high estragole concentrations, P450 2C19, 2D6, and 2E1 might contribute to some extent. Comparison to results from similar studies for safrole and methyleugenol revealed that competitive interactions between estragole and methyleugenol 1'-hydroxylation and between estragole and safrole 1'-hydroxylation are to be expected because of the involvement of, respectively, P450 1A2 and P450 2A6 in the bioactivation of these compounds. Furthermore, poor metabolizer phenotypes in P450 2A6 might diminish the chances on bioactivation of estragole and safrole, whereas lifestyle factors increasing P450 1A2 activities such as cigarette smoking and consumption of charbroiled food might increase those chances for estragole and methyleugenol.

CYP1A1, an enzyme of the cytochrome P450 superfamily, is the most important xenobiotic-metabolizing enzyme of the placenta for which relevant inducible activity has been demonstrated throughout pregnancy. CYP1A1 metabolizes several drugs and compounds widely used in pharmacotherapy or present in diets. At the same time, this enzyme plays a key role in the bioactivation of procarcinogens and proteratogens, such as arylamines and polycyclic aromatic hydrocarbons (PAHs), which bind to placental and foetal DNA as DNA-adducts. The expression of CYP1A1 is transcriptionally up-regulated through the ligand-activated aryl hydrocarbon receptor (AhR). AhR plays an important role as mediator of an adaptive response to xenobiotics, as well as in normal physiology and embryonic development. Several exogenous AhR ligands, such as PAHs, polychlorinated biphenyls and halogenated dioxins, can be found in the constituents of numerous commercial products, including insulators and flame retardants, or as products of combustion processes, including chimney soot, charbroiled foods and cigarette smoke, or as the product of waste incineration. Exposure to these compounds subsequently affects cellular growth and differentiation, homeostasis, level of growth factors, reproduction function and hormonal regulation. Importantly, elevated CYP1A1 activity through activated AhR in placentas of women smokers has been associated with pregnancy complications, such as premature birth, intrauterine growth retardation (IUGR), structural abnormalities, foetal death or placenta abruption, risk of low birth weight, low birth length and low head circumference. We summarize the recent findings related to toxicological consequences of AhR activation and CYP1A1 induction in the human placenta during pregnancy.

Vitamin A appears to exert a protective effect against certain cancers. Epithelial cancers, such as those of the skin, bladder, oropharynx and respiratory tract, have the strongest association with vitamin A. These same cancers are causally associated with exposure to carcinogens such as benzo(alpha)pyrene (BP), a product of combustion found in cigarette smoke and charbroiled meat. This study was designed to determine whether BP exposure affects tissue vitamin A nutriture. Female Sprague-Dawley rats were randomized to purified diets, sufficient or deficient in vitamin A, and with or without 200 mg BP/kg feed. Rats were killed after 4 or 6 weeks. Serum, liver and lungs were assessed for vitamin A levels; trachea, stomach, small intestine and bladder were examined for histologic change. Lack of dietary vitamin A resulted in a profound decrease in vitamin A in the serum, liver and lungs (p less than .005). No histologic changes were evident in any tissues examined. Serum vitamin A was not affected by dietary BP. In vitamin-A-sufficient rats, dietary BP caused a significant decline in hepatic and lung vitamin A. In rats fed vitamin-A-deficient diets, dietary BP had no effect on tissue vitamin A. We conclude that chronic exposure to the carcinogen BP leads to tissue depletion of vitamin A, despite a vitamin-A-sufficient diet. We postulate that BP impairs tissue repletion by metabolizing incoming vitamin A rather than in situ vitamin A, since BP had no effect on tissue vitamin A levels in rats fed a diet devoid of vitamin A. This BP-induced vitamin depletion may eventually have a deleterious effect on epithelial tissue health, and may help to explain the association between vitamin A and cigarette-smoke-related cancers.

Heterocyclic aromatic amines are sometimes formed during the cooking of muscle meats, and their mutagenic and carcinogenic effects are of potential concern in the aetiology of human cancer. In a large survey of the heterocyclic amine content of foods, fried or charbroiled hamburgers, fried chicken, chicken breast sandwiches, fish sandwiches and breakfast sausages were purchased from fast-food restaurants. At least three different chains were visited per product and samples from five stores from each chain were pooled. The solid-phase extraction and HPLC method was used to analyse pooled samples for heterocyclic amine content and mutagenic activity with the Ames/Salmonella assay. Samples were analysed in a blind study which also contained quality control samples of two types, one high and one low in heterocyclic amine content and mutagenic activity. Results from the fast-food products showed undetectable levels of heterocyclic amines in 10 of 17 samples and only low levels [< or = 1 ng/g total of 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx), 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) and 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline (DiMeIQx)] in the remaining samples. Compared with literature values based primarily on laboratory and home cooking conditions, fast-food meat products appear to contribute only a small percentage of the estimated daily dietary intake of heterocyclic amines.