Analysis and health risk assessment of priority gaseous polycyclic aromatic hydrocarbons during meat frying: A mathematical modelling

ABSTRACTDeep-fried dough sticks (a Chinese traditional breakfast) were fried individually in peanut, sunflower, rapeseed, rice bran, soybean and palm oil without any time lag for 32 h (64 batches fried, each for 30 min) and fried oil samples were obtained every 2 h. The frying-induced changes in the levels of total polar compounds (TPC) and polycyclic aromatic hydrocarbons (PAHs) were investigated by edible oil polar compounds (EOPC) fast separation chromatographic system and gas chromatography-mass spectrometry (GC-MS), respectively. The correlations were analysed of TPC with benzo[a]pyrene (BaP), TPC and PAH4 (benzo[a]anthracene, chrysene, benzo[b]fluoranthene and benzo[a]pyrene) as well as TPC with PAH16 (USEPA 16 PAHs). The results revealed that the levels of TPC and PAHs in fried oil considerably increased with frying time, and the type of oil affected their formation, which could inform the choice of oil for frying. The total BaP equivalents (∑BaPeq) concentrations in fresh oil and in oil whose TPC exceeded 27% were 2.14–13.48 and 5.78–10.80 μg kg–1, respectively, which means that the carcinogenic potency of frying oil was more pronounced than that of fresh oil. In addition, the TPC concentration was significantly correlated with the concentrations of the sum of the 16 PAHs, PAH4 and BaP, so that the levels of PAHs could be predicted according to the levels of TPC in fried oil. In European standards, the rejection point for TPC in frying oil should be recalculated when considered PAHs. In all, the concentration of PAHs is a vital factor for ensuring the safety of frying oil.

Polycyclic aromatic hydrocarbons (PAHs) content of edible vegetable oils in Iran: A risk assessment study

Background: Inhalation is one of the main means of human exposure to polycyclic aromatic hydrocarbons (PAHs) because of their ubiquitous presence in the atmosphere. However, most studies have considered only PAHs found in the particle phase and have omitted the contribution of the gas-phase PAHs to the risk.Objective: We estimated the lifetime lung cancer risk from PAH exposure by inhalation in people living next to the largest chemical site in Southern Europe and the Mediterranean area.Methods: We determined 18 PAHs in the atmospheric gas and particle phase. We monitored the PAHs for 1 year in three locations near the chemical site in different seasons. We used toxic equivalence factors to calculate benzo[a]pyrene (BaP) equivalents (BaP-eq) for individual PAHs and applied the World Health Organization unit risk (UR) for BaP (UR = 8.7 × 10–5) to estimate lifetime cancer risks due to PAH exposures.Results: We observed some spatial and seasonal variability in PAH concentrations. The contribution of gas-phase PAHs to the total BaP-eq value was between 34% and 86%. The total estimated average lifetime lung cancer risk due to PAH exposure in the study area was 1.2 × 10–4.Conclusions: The estimated risk was higher than values recommended by the World Health Organization and U.S. Environmental Protection Agency but lower than the threshold value of 10–3 that is considered an indication of definite risk according to similar risk studies. The results also showed that risk may be underestimated if the contributions of gas-phase PAHs are not considered.

BackgroundPolycyclic aromatic hydrocarbons (PAHs) are the main toxic compounds in natural bitumen, a fossil material used by modern and ancient societies around the world. The adverse health effects of PAHs on modern humans are well established, but their health impacts on past populations are unclear. It has previously been suggested that a prehistoric health decline among the native people living on the California Channel Islands may have been related to PAH exposure. Here, we assess the potential health risks of PAH exposure from the use and manufacture of bitumen-coated water bottles by ancient California Indian societies.MethodsWe replicated prehistoric bitumen-coated water bottles with traditional materials and techniques of California Indians, based on ethnographic and archaeological evidence. In order to estimate PAH exposure related to water bottle manufacture and use, we conducted controlled experiments to measure PAH contamination 1) in air during the manufacturing process and 2) in water and olive oil stored in a completed bottle for varying periods of time. Samples were analyzed with gas chromatography/mass spectrometry (GC/MS) for concentrations of the 16 PAHs identified by the US Environmental Protection Agency (EPA) as priority pollutants.ResultsEight PAHs were detected in concentrations of 1–10 μg/m3 in air during bottle production and 50–900 ng/L in water after 2 months of storage, ranging from two-ring (naphthalene and methylnaphthalene) to four-ring (fluoranthene) molecules. All 16 PAHs analyzed were detected in olive oil after 2 days (2 to 35 μg/kg), 2 weeks (3 to 66 μg/kg), and 2 months (5 to 140 μg/kg) of storage.ConclusionsFor ancient California Indians, water stored in bitumen-coated water bottles was not a significant source of PAH exposure, but production of such bottles could have resulted in harmful airborne PAH exposure.

Many workers are occupationally exposed to polycyclic aromatic hydrocarbons (PAHs), which may cause various health problems, and some PAHs are known or suspected carcinogens. PAH exposure is primarily monitored by air sampling, but contamination may also occur through dermal exposure. PAHs adsorbed to the skin can be sampled by tape-stripping, but subsequent extraction of sampling tapes in organic solvent also releases diverse co-eluting substances that are difficult to remove before analysis of the PAHs by gas chromatography/mass spectrometry (GC/MS). The objective of this study was to optimise a procedure for analytical clean-up after extraction of 32 PAHs from tape-strips, by dialysis in organic solvent using semipermeable membranes. With triplicate subsamples, the developed method yields acceptable precision and repeatability for both the 32 PAHs, across the concentration range 10–160 ng per sample, and for a certified reference material (urban dust). The optimized clean-up procedure and GC/MS methodology was used to assess PAHs on skin from the lower part of the ventral side of the wrist and just below the collar bone of three firefighters and seven controls (office workers). Several gaseous and particle-bound PAHs were detected in all samples, including controls. Thus, the optimized procedure using semipermeable membranes for clean-up of tape-strip extracts can be used to assess the dermal exposure of both occupational and general populations to multiple PAHs. The results also show that both gaseous and particle-bound PAHs, including alkylated species, may be present on skin.

Polycyclic aromatic hydrocarbons in gas and particulate phases of indoor environments influenced by tobacco smoke: Levels, phase distributions, and health risks

A review of monitoring of airborne polycyclic aromatic hydrocarbons: An African perspective

Modeling the exposure functions of atmospheric polycyclic aromatic hydrocarbon mixtures in occupational environments.

Characteristics of Exposure Profiles for Workers Exposed to Airborne Dusts and Polycyclic Aromatic Hydrocarbons (PAHs) in the Carbon Black Manufacturing Industry: Perng‐Jy Tsai, et al. Department of Environmental and Occupational Health, Medical College, National Cheng Kung University—This study was aimed at characterizing the exposure profiles for carbon black manufacturing workers. Personal sampling was conducted on 8 wet pelletizing workers and 22 packaging workers. A sampling train consisted of an IOM personal inhalable aerosol sampler (to collect airborne dusts and their inherent particle‐bound polycyclic aromatic hydrocarbons (PAHs)), and an XAD‐2 sorbent tube (to collect gaseous PAHs) was used. For PAHs analyses, 21 PAH species were analyzed by using the gas chromatograph/mass technique. In addition, size segregating sampling was conducted at both workplaces, by using both the Micro‐orifice Uniform Deposited Impactors (MOUDI) and the Noll Rotary Impactor (NRI) simultaneously to characterize the particle size distributions exposure to both exposure groups. Results show that the packaging workers had a higher dust exposure level (arithmetic mean=1.17 mg/m3) than the pelletizing workers (arithmetic mean=0.82 mg/m3). Although both levels were lower than the time‐weighted‐average threshold limit value (TLV‐TWA) of 3.5 mg/m3 of ACGIH, about 7.48% of the packaging workers were estimated to be above the limit value. A significant amount of gaseous PAHs was also found in personal exposure, especially BaP and PER in the gaseous phase were similar to those found in the particle‐bound phase. Exposure to particle‐bound PAHs was considered due to the releasing of carbon black dusts during the pelletizing and packaging processes, but for gaseous PAHs, it might be due to the emission of gaseous PAHs from the feedstock oil unloading process rather than the stack flue gas. The above findings suggest that both gaseous and particle‐bound PAHs are equally important in assessing exposure of carbon black industry workers. Size distributions, including both airborne dusts and particle‐bound PAHs, collected from both areas were found in the form of bimodality. No statistical difference could be found between the airborne dust size distribution and the corresponding particle‐bound PAH size distribution in the two areas, which suggests that workers in both areas might be exposed to similar types of airborne dust that contain similar PAH compositions.

Cooking activities are an important source of indoor air pollution which contributes significantly to Polycyclic Aromatic Hydrocarbons (PAHs) in the environment. This study investigated sixteen (16) priority PAHs emitted from smoke in eight (8) cooking fuels commonly used in Nigeria. Gas Chromatography Mass Spectrometry (GC-MS) was used for sample analysis and the potential health risk associated with exposure to PAHs were evaluated. The highest total quantified PAHs concentration was obtained from the burning of palm kernel fiber with an average ΣPAHs of 14.06 mg/kg. The result showed a variation in the average concentration of 10.82 − 14.06 mg/kg for all the cooking fuels. 3-ringed PAHs were found to be the dominant PAHs in the samples considered in terms of concentrations and frequency of occurrence at 7.03-9.42 mg/kg. Benzo[a]anthracene was the most abundant PAHs in biomass materials while Benzo[a]pyrene was the most abundant in liquified petroleum gas and Benzo[b]fluoranthene in kerosene. The cancer risk for both the children and adult obtained for all the cooking fuel samples were less than 10 − 6 which is satisfactory except in sawdust which has a value of 1.30 × 10 − 5 and 1.44 × 10 − 5 for child and adult, respectively. It is recommended that cleaner cooking fuels be used in well-ventilated environments to reduce exposure to these pollutants. Highlights Sixteen priority PAHs in emissions from the burning of eight cooking fuels in Nigeria were investigated Emission sources of the PAHs were identified using diagnostic ratios Health risks of PAHs in emissions from the burning of cooking fuels is higher in adult

Polycyclic aromatic hydrocarbons (PAHs) are well-known hazardous substances; nevertheless, research on their exposure and health concerns associated with kerosene fuel emissions is limited. In this study, PAH (combined gaseous and particle phase) monitoring was carried out in the kitchen and living room in selected households. Personal exposure and cooking time monitoring were also carried out, simultaneously. The study's findings revealed that BaP, BA, BbF, and Nap were the most prevalent PAHs in both the summer and winter seasons, regardless of urban or rural households. The estimated values of average incremental lifetime cancer risks were found to be greater than the USEPA level, i.e., 1 × 10-6, in both urban and rural households, regardless of seasonal fluctuation. In both seasons, the non-carcinogenic risk for developmental and reproductive effects was higher in rural women than in urban women, and in case of developmental risk it showed greater than unity (rural: 1.11 and urban 1.03) in the winter season. On the other hand, Monte Carlo simulation model revealed that concentrations of PAHs (97.1% and 97.5%) and exposure duration (51.7% and 56.7%) were the most sensitive factors contributed for health risk estimations for urban and rural area in both seasons, respectively. Furthermore, the results clearly showed that women who were using kerosene for cooking were at a greater risk of acquiring both carcinogenic and non-carcinogenic health consequences from PAH exposure from kerosene cookstoves. It was recommended that they should utilize clean fuel, either by using LPG under the PMUY scheme or by using electricity/solar power to reduce health risks for better health.

Background: Polycyclic aromatic hydrocarbons (PAHs) are a class of chemicals common in the environment. Major sources of PAHs include fossil fuel combustion and cigarette smoking. Certain PAHs are carcinogenic, though the degree to which genetic variation influences susceptibility to PAH exposure remains unclear. Benzo(a)pyrene (BaP) is a well-studied PAH that is classified as a probable human carcinogen. Here, we evaluated haplotype frequency in genes related to PAH metabolism and detoxification, and explored the interactions between PAH exposure and haplotype on BaP-DNA adducts, an established cancer risk marker, in umbilical cord white blood cells (WBCs). Methods: Maternal and umbilical cord blood were collected at delivery from participants in a longitudinal cohort study of African American (AA) and Dominican (D) mothers and newborns in New York City. WBC DNA was isolated from cord blood, and genetic polymorphisms and BaP-DNA cord adducts were then measured in 516 mothers and 323 newborns. Maternal PAH exposure was measured during pregnancy with a personal air exposure monitor. A total of 18 genes, selected for biologic relevance, were analyzed for SNPs. For this study, a subset of 7 maternal and newborn genes related to PAH metabolism, detoxification and repair were selected for haplotype analyses: CYP1A1, CYP1A2, CYP1B1, GSTM, GSTT, NQO1 and XRCC. Haplotype × PAH interactions on logarithmic-transformed BaP-DNA adduct levels were explored. Results: Notable differences in haplotype frequency were observed between AAs and Ds and between mothers and newborns. We observed a number of significant interactions between high PAH exposure and polymorphic haplotypes in both mothers and newborns on BaP-DNA adducts in cord blood. To give one example, the haplotype CACGCG of CYP1B1 in AA mothers had a frequency of 10.4%, versus 0.3% in D mothers (p<0.0001). By comparison, the reference haplotype TAGCTG had a frequency of 19.9%. We observed a significant interaction between the CYP1B1 haplotype and high PAH exposure on cord BaP-DNA adducts in AA newborns (β=−0.67, p=0.01) but not Ds (β=−0.13, p=0.72). We will present results for both maternal and newborn CYP1A1, CYP1A2, GSTM, GSTT, NQO1 and XRCC haplotypes in both AAs and Ds. Discussion: It is biologically plausible that an individual's ability to metabolically activate and detoxify BaP and repair DNA damage plays a role in susceptibility to DNA adduct formation following prenatal PAH exposure. Ultimately, this susceptibility could correlate with future risk of cancer development. We have identified haplotype patterns that differ between ethnic groups and also between mothers and newborns. We also observed several haplotype × PAH exposure interactions on cord BaP-DNA adducts, supporting the hypothesis that genetic variability can contribute to susceptibility and potential cancer risk from prenatal PAH exposures. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2753. doi:10.1158/1538-7445.AM2011-2753

B45 Polycyclic aromatic hydrocarbons (PAHs) are widespread organic carcinogenic pollutants. When metabolized in vivo, PAHs form reactive diol epoxides that bind to DNA at guanine residues forming adducts. PAH exposure has also been associated with alterations in genomic cytosine methylation. Both PAH-DNA adducts and altered DNA methylation have been associated with increased cancer risk. We sought to explore the relationship between prenatal PAH exposure, global DNA methylation and PAH-DNA adducts in a New York City birth cohort. Cord blood was collected from deliveries of non-smoking, African Americans and Dominicans, ages 18-35, residing in N. Manhattan and S. Bronx. Personal air monitors measured PAH during their 8th month of pregnancy. We measured benzo[a]pyrene (B[a]P)-DNA adducts (which serve as a proxy for PAH-DNA adducts) in cord blood using high-performance liquid chromatography-fluorescence. We measured genomic DNA methylation in cord blood leukocytes using the MethylampTM global DNA methylation quantification kit. Demographic and epidemiologic risk factors were collected prospectively, including maternal age, ethnicity, parity, and prenatal tobacco smoke exposure, and child’s gender We found that prenatal PAH exposure was associated global DNA hypomethylation such that average methylation among those in the highest quartile of prenatal PAH exposure was 1.17 ng/100 ng total DNA as compared 1.83 ng/100 ng total DNA in the lowest quartile (p < 0.01). Conversely, those with detectable PAH-DNA adducts had higher levels of DNA methylation (1.43 ng/100 ng total DNA) as compared to those with non-detectable adducts (1.16 ng/100 ng total DNA) (p = 0.02). Using multiple variable linear regression, PAH exposure was independently associated with hypomethylation (average difference in methylation among those in the highest vs. lowest quartile of exposure = -0.42, 95% CI: -0.75, -0.09) and the presence of DNA adducts was associated with hypermethyaltion (average difference in methylation among those with detectable vs. non-detectable adducts = 0.28, 95% CI: 0.05, 0.49). Adjusting for potential confounders did not significantly alter these independent associations, indicating that the lowest level of global DNA methylation was found among those with non-detectable adducts and high PAH exposure, and the highest level of DNA methylation was found among those with detectable adducts and low PAH exposure. While the mechanism by which prenatal PAH exposure results in DNA adducts is well understood, the way exposure may impact methylation is not known. These data suggest that in the presence of DNA adducts, PAH exposure is associated with a reduction in methylation, but when adducts are non-detectable, the same PAH exposure is associated with an even larger methylation reduction. It is possible that the presence of adducts may be partially preventing PAH compounds (or metabolites) from accessing the DNA, leading to less of a change in methylation. It is also possible that the shift in global methylation from PAH exposure may prevent adduct formation. These speculations as well as the associations observed in this analysis require confirmation in other settings/populations. Because methylation changes are potentially reversible, it is possible that if these associations are confirmed, methylation may serve as a target for intervention. Citation Information: Cancer Prev Res 2008;1(7 Suppl):B45.

多環芳香烴碳氫化合物(polycyclic aromatic hydrocarbons，PAHs)為常見之空氣污染物，各種與PAHs暴露相關的職業如煉焦業、鑄造業、電弧爐業等得到相關癌症的危險性相對來說比其他行業高。鑄造業為工業之母，有其必要性去探討此環境中PAHs分佈特性及勞工個人暴露情形。本研究針對作業場所進行粒徑分佈採樣、勞工個人PAHs採樣及生物偵測評估，探討不同粒徑下PAHs的濃度分佈，並研究勞工暴露之氣/固相PAHs情形，且進行外在暴露與體內代謝物(1-hydroxypyrene，1-OHP)、氧化損傷(8-OHdG)及DNA鍵結物(N7-methylguanine，N7-MeG)之相關性探討。結果顯示四個工作區中，可呼吸性粉塵(<4 μm)之PAHs濃度佔總粉塵的48 %~95 %，且大部份的PAHs質量濃度集中在細微粒部分(<1 μm)，又以高分子量PAHs居多，故其危害性更大。而氣/固相分析結果指出，勞工所暴露之PAHs以氣相為主要暴露源，以二和三環PAHs為主。在生物偵測方面，發現鑄造業勞工尿中1-OHP濃度顯著高於控制組，但氧化損傷與環境暴露的相關性較弱。在致肺癌之健康風險評估方面，爐區與澆鑄區屬於高暴露區域，其推算出來之風險限值大於OSHA訂定的10-3，因此有必要加強鑄造業勞工之呼吸暴露防範，將職場危害性降至最低。

This study aimed to investigate the association between particulate PAHs exposure and DNA damage in Malaysian schoolchildren in heavy traffic (HT) and low traffic (LT) areas. PAH samples at eight schools were collected using a low volume sampler for 24 h and quantified using Gas Chromatography-Mass Spectrometry. Two hundred and twenty-eight buccal cells of children were assessed for DNA damage using Comet Assay. Monte-Carlo simulation was performed to determine incremental lifetime cancer risk (ILCR) and to check the uncertainty and sensitivity of the estimated risk. Total PAH concentrations in the schools in HT area were higher than LT area ranging from 4.4 to 5.76 ng m−3 and 1.36 to 3.79 ng m−3, respectively. The source diagnostic ratio showed that PAHs in the HT area is pyrogenic, mainly from diesel emission. The 95th percentile of the ILCR for children in HT and LT area were 2.80 × 10−7 and 1.43 × 10−7, respectively. The degree of DNA damage was significantly more severe in children in the HT group compared to LT group. This study shows that total indoor PAH exposure was the most significant factor that influenced the DNA damage among children. Further investigation of the relationship between PAH exposure and genomic integrity in children is required to shed additional light on potential health risks.