The aim of this study was to assess potential health risks among children and adolescents consuming various grilled marshmallows using a survey and to determine polycyclic aromatic hydrocarbons (PAHs) in these food products. PAH analysis in grilled marshmallows included a dilution stage with deionized water and liquid-liquid extraction with cyclohexane and solid-phase extraction (SPE). PAH fractions were initially analyzed via high-performance thin-layer chromatography, and PAH concentrations were determined via gas chromatography with a tandem mass detector using the selective reaction monitoring (SRM) mode. This study on the consumption of grilled marshmallows was conducted among approximately 300 children and adolescents. The preliminary results indicated that \"raw\" marshmallows did not contain PAHs. However, the obtained data suggested the exposure of young people to carcinogenic PAHs from grilled marshmallows (63.5% of them consumed marshmallows). Carcinogenic benzo(a)pyrene (BaP) was determined in all samples. The profile of PAH concentrations in the extracts isolated from various grilled types of marshmallows was similar (r2 > 0.8000), regardless of the grilling method. Compared to the white sugar confection, higher concentrations of PAHs were determined in multicolored marshmallows. The lack of social awareness about exposure to carcinogenic substances is alarming.

We evaluated spatial distribution and source apportionment of polycyclic aromatic hydrocarbons (PAHs) in water and sediments at four selected sites of the Ganga River. Also, we measured PAHs in muscle tissues of Rohu (Labeo rohita), the most common edible carp fish of the Ganga River and potential human health risk was addressed. Total concentration of PAHs (∑PAHs) in water was highest at Manika Site (1470.5 ng/L) followed by Knuj (630.0 ng/L) and lowest at Adpr (219.0 ng/L). A similar trend was observed for sediments with highest concentration of ∑PAHs at Manika (461.8 ng/g) and lowest at Adpr Site (94.59 ng/g). Among PAHs, phenanthrene (Phe) showed highest concentration in both water and sediment. Of the eight major carcinogenic contributors (∑PAH8C), Indeno (1,2,3-C,D) pyrene (InP) did appear the most dominant component accounting for 42% to this group at Manika Site. Isomer ratios indicated vehicular emission and biomass combustion as major sources of PAHs. The ∑PAHs concentrations in fish tissue ranged from 117.8 to 758.0 ng/g (fresh weight basis) where low molecular weight PAHs assumed predominance (above 80%). The risk level in fish tissues appeared highest at Manika Site and site-wise differences were statistically significant (p < 0.05). The ILCR (> 10-4) indicated carcinogenic risk in adults and children associated with BaP and DBahA at Manika Site and with BaP at Knuj Site. Overall, the concentrations exceeding permissible limit, carcinogenic potential and BaP equivalent all indicated carcinogenic risks associated with some individual PAHs. This merits attention because the Ganga River is a reservoir of fisheries.

The northern Gulf of Mexico has a long history of polycyclic aromatic hydrocarbon (PAH) contamination from anthropogenic activities, natural oil seepages, and the 2010 Deepwater Horizon explosion and oil spill. The continental shelf of the same area is a known breeding ground for sperm whales (Physeter macrocephalus). To evaluate PAH-DNA damage, a biomarker for potential cancer risk, we compared skin biopsies collected from Gulf of Mexico sperm whales in 2012 with skin biopsies collected from sperm whales in areas of the Pacific Ocean in 1999-2001. All samples were obtained by crossbow and comprised both epidermis and subcutaneous blubber. To evaluate exposure, 7 carcinogenic PAHs were analyzed in lipids extracted from Pacific Ocean sperm whale blubber, pooled by sex, and location. To evaluate PAH-DNA damage, portions of all tissue samples were formalin-fixed, paraffin-embedded, sectioned, and examined for PAH-DNA adducts by immunohistochemistry (IHC) using an antiserum elicited against benzo[a]pyrene-modified DNA, which crossreacts with several high molecular weight carcinogenic PAHs bound to DNA. The IHC showed widespread epidermal nuclear localization of PAH-DNA adducts in the Gulf of Mexico whales (n = 15) but not in the Pacific Ocean whales (n = 4). A standard semiquantitative scoring system revealed significantly higher PAH-DNA adducts in the Gulf of Mexico whales compared to the whales from the Pacific Ocean study (p = .0002).

The occurrence of atmospheric fine particles (PM2.5)-associated polycyclic aromatic hydrocarbons (PAHs), trace metals and organic molecular markers was investigated by conducting an intensive sampling campaign at the Eastern Mediterranean urban area of Nicosia (Cyprus). Sixty-two 24-hr PM2.5 samples were collected and analyzed for fifty parent and alkylated PAHs, twenty-five long chain n-alkanes, seventeen hopanes and twelve steranes used for source apportionment. The same number and kind of samples were analyzed to determine twenty-eight trace metals. Emphasis was given to investigate the air levels of the scarcely monitored although highly carcinogenic PAHs such as dibenzopyrenes, dibenzoanthracenes, 7H-benzo[c]fluorene and 5-methyl-chrysene, not included in the USEPA\'s sixteen PAH priority list (USEPA-16). UNMIX receptor model was applied to apportion the sources of atmospheric emissions of the determined organic compounds and trace metals and evaluate their daily contributions to the corresponding PM2.5 associated concentrations. For comparison purposes, principal component analysis with multiple linear regression (PCA/MLR) was also applied and its results are reported. The UNMIX receptor model, compared to PCA/MLR, offered a more precise source profile and more reliable daily mass source distributions by eliminating negative contributions. The individual and cumulative multi-pathway lifetime cancer risk (posed via inhalation, ingestion and dermal contact) by exposure to PM2.5-associated USEPA-16 listed and non-listed PAHs and selected airborne trace metals (As, Cd, Co, Ni, and Pb) were assessed. To estimate the contribution of each emission source to the total cancer risk, multiple linear regression analysis was performed, using as independent variables the daily source mass contributions and as dependent variables the respective cancer risk units. The estimated total cumulative cancer risk comprising all toxic PAHs, besides those included in the priority list, and metals was higher than the USEPA\'s threshold by a factor of eight, denoting a potential risk for long-term exposure of a population in the urban environment.

The toxicities of many environmental polycyclic aromatic hydrocarbons (PAHs), in particular those of high-molecular-weight PAHs (with MW higher than 300), remain poorly characterized. The objective of this study was to evaluate the ability of selected environmentally relevant PAHs with MW 302 (MW302 PAHs) to activate the aryl hydrocarbon receptor (AhR), since this represents a major toxic mode of action of PAHs. A large number of the evaluated compounds exhibited strong AhR-mediated activities, in particular in human models. The studied MW302 PAHs also significantly contributed to the overall calculated AhR activities of complex environmental mixtures, including both defined standard reference materials and collected diesel exhaust particles. The high AhR-mediated activities of representative MW302 PAHs, e.g. naphtho[1,2-k]fluoranthene, corresponded with the modulation of expression of relevant AhR target genes in a human lung cell model, or with the AhR-dependent suppression of cell cycle progression/proliferation in estrogen-sensitive cells. This was in a marked contrast with the limited genotoxicity of the same compound(s). Given the substantial levels of the AhR-activating MW302 PAHs in combustion particles, it seems important to continue to investigate the toxic modes of action of this large group of PAHs associated with airborne particulate matter.

This study was conducted to investigate the concentrations, distributions, toxicities, and sources of polycyclic aromatic hydrocarbons (PAHs) in the soils from different areas in Ulsan, South Korea. Samples were collected from 41 sites, including a waste treatment facilities area (WA), traffic facilities area (TA), child playground area (CA), industrial area (IA), railroad facilities area (RA), ore and iron scraps fields area (OA), and residential area (ReA). Ulsan was chosen for research area because it used to be an environmental hot spot in South Korea, and 16 PAHs in the US EPA priority pollutant list were selected. The concentration of total PAHs (t-PAHs) ranged from 61.7 to 12,421 μg/kg, and the average concentration of t-PAHs was 706.9 μg/kg. The distribution of PAHs by ring number indicated that the portion followed the order of 4 rings > 5 rings > 3 rings > 6 rings > 2 rings. According to PAH origin indices, LMW/HMW (low molecular weight 2-3 ring PAHs over high molecular weight 4-6-ring PAHs), phenanthrene/anthracene ratio and fluoranthene/pyrene ratio, benzo(g,h,i)perylene/indeno (1,2,3-c,d)pyrene ratio, vehicular emissions, and the combustion of fossil fuel were the sources of PAHs. The strong correlation (R2 = 0.995) between t-PAHs and total carcinogenic PAHs (t-PAHcarc) indicated that the concentration of t-PAHcarc increased in proportion with that of t-PAHs. The toxic equivalent concentrations (TEQs) of PAHs in the soils ranged from 44.0 to 1929.9 μg TEQ/kg. It is imperative to set regulatory levels for PAHs for periodic monitoring and rapid remediation action of contaminated soils, because there are no national standards in South Korea for 15 PAHs with the exception of benzo(a)pyrene.

A study on vertical distribution of magnetic susceptibility, carcinogenic and endocrine disrupting PAHs was performed in the reclaimed mudflat sediments adjacent to the Thane Creek of Mumbai. The 5-rings PAHs and ΣC-PAHs were more dominant at 120cm depth contributing 52.23% and 60.19% respectively to ∑PAHs. The average ratio values of LMW/HMW PAHs (0.58); Fla/(Fla+Pyr) (0.50); Ant/(Ant+Phe) (0.50); BaA/(Chry+BaA) (0.48); BaP/BghiP (2.06), Phe/Ant (1.03) and BaA/Chr (0.93) indicate that the PAH contamination might have raised due to inefficient combustion and pyrogenic emissions during the open burning of solid waste in the vicinity. This was further supported by the anthropogenic ferri(o)magnetic loading over the last 100years influencing the Creek sediments. The PAHs toxicity estimation was performed by calculating the toxic equivalent quantity (TEQ) value of 8.62ng TEQ/g which was below the safe level (600ng TEQ/g) suggested by the Canadian risk-based soil criterion for protection of human health.

This study investigated the levels, sources and potential risks of 17 polycyclic aromatic hydrocarbons in surface sediment samples collected along the Mithi River of Mumbai. The concentration level of ΣPAHs found in the present study was in the range of 1206-4735 ng/g dw. The composition patterns of PAHs by ring size in sediment were surveyed which indicate the dominance of four rings followed by five and three ring PAHs. In the study it was observed that the high molecular weight PAHs (HMW PAHs) made greater contributions of 90.83% as compared to that of low molecular PAHs (LMW PAHs) contributing to 9.17% to the total PAH concentrations. Toxicity and biological risk were assessed using toxic equivalent quantity and sediment quality guideline quotient. It is feared that the pollution level of PAHs in the sediments might increase in coming times resulting in an unconspicuous risks for the environment and humans through food chains.

Risk-based, background, and laboratory quantitation limit-derived standards for carcinogenic polycyclic aromatic hydrocarbons (cPAHs) in residential and nonresidential soils vary across the northeast region of the United States. The magnitude and extent of this variation, however, have not been systematically studied. This article examines the technical basis and methodology used by eight northeastern states in the development of risk-based screening values, guidelines, and standards for cPAHs in soils. Exposure pathways, human receptors, algorithms, and input variables used by each state in the calculation of acceptable human health risks are identified and reviewed within the context of environmental policy and regulatory impacts. Emphasis is placed on a comparative analysis of multipathway exposures (incidental ingestion, dermal contact, and particulate inhalation) and key science-policy decisions that have led to the promulgation and adoption of different exposure criteria for cPAHs in the Northeast. More than 425 data points and 20 distinct exposure factors across eight state programs, 18 age subgroups, six activity scenarios, and three exposure pathways were systematically evaluated. Risk-based values for one state varied either above or below risk-based, background or laboratory quantitation limit-derived standards of another state for the same cPAH and receptor. Standards for cPAHs in soils were found to differ significantly across the northeast region--in some cases, by one or two orders of magnitude. While interstate differences can be expected to persist, future changes in federal guidance could mean a shift in risk drivers, compliance status, or calculated cumulative risks for individual properties impacted by PAH releases.

OBJECTIVE: Relative importance of multiple indoor and outdoor venues on personal exposure concentrations to pro-carcinogenic polycyclic aromatic hydrocarbons (c-PAHs) remains poorly understood. This is particularly challenging because many c-PAHs share sources and occur as a complex mixture. Accurate and precise apportionment of personal exposure according to exposure venues could aid in the understanding of human health effects due to a given source. Here, we partitioned indoor and personal exposure concentrations to seven c-PAHs and pyrene according to the indoor- and outdoor-origins.
METHODS: A simultaneous, integrated monitoring of personal, indoor and outdoor concentrations of nine PAHs was conducted in 75 homes for a consecutive 48-hour period across a two-year period in Kraków, Poland. Due to few known indoor sources for chrysene, we used this PAH species as a tracer for infiltration of outdoor PAHs. Personal and indoor concentrations of seven c-PAHs and pyrene were apportioned to home indoor, non-home indoor and outdoor origins.
RESULTS: Using Chrysenein/Chryseneout as proxy for an infiltration factor, Finf, infiltrated PAHs of outdoor origin are overall higher in concentration than those emitted from the indoor origin. Average contribution by the outdoor sources on B[a]A, B[b]F, and B[k]F were 92%, 79%, and 78% across all seasons, respectively. In contrast, in homes where a household member smoked, average contributions by the outdoor sources on B[ghi]P, B[a]P, D[ah]A, and IP were lower (i.e., 67%, 65%, 67%, and 66%, respectively). Season-averaged contributions by the outdoor sources on personal exposure to B[a]A, B[b]F, and B[k]F were 92%, 74%, and 77%, respectively. On the other hand, season-averaged home indoor source contributions on personal exposure to B[a]A, B[b]F, and B[k]F were estimated at 6%, 15%, and 19%, respectively. Similar contributions by season-averaged home indoor sources on personal exposure were estimated at 28% for B[ghi]P, 31% for B[a]P, 25% for D[ah]A, and 28% for IP.
CONCLUSIONS: Of the seven c-PAHs, B[a]A, B[b]F, and B[k]F are enriched in indoor and personal exposure concentrations from the outdoor coal-combustion. B[ghi]P, B[a]P, D[a,h]A, and IP, PAHs with some of the highest carcinogenic and mutagenic potencies, are considerably enriched by cigarette smoke in addition to the outdoor sources.