High Polycyclic Aromatic Hydrocarbons Exposure Research Articles

Prenatal Exposure to Air Pollution, Maternal Psychological Distress, and Child Behavior

Airborne polycyclic aromatic hydrocarbons (PAHs) are pollutants generated by combustion of fossil fuel and other organic material. Both prenatal PAH exposure and maternal psychological distress during pregnancy have each been associated with neurodevelopmental problems in children. The goal was to evaluate potential interactions between prenatal exposure to airborne PAHs and maternal psychological distress during pregnancy on subsequent behavioral problems in children. In a longitudinal birth cohort study, 248 children of nonsmoking white women in the coal-burning region of Krakow, Poland, were followed from in utero until age 9. Prenatal PAH exposure was measured by personal air monitoring during pregnancy, maternal demoralization during pregnancy by the Psychiatric Epidemiology Research Instrument-Demoralization, and child behavior by the Child Behavior Checklist. Significant interactions between maternal demoralization and PAH exposure (high versus low) were identified for symptoms of anxious/depressed, withdrawn/depressed, social problems, aggressive behavior, internalizing problems, and externalizing problems. The effects of demoralization on syndromes of anxious/depressed, withdrawn/depressed, rule-breaking, aggressive behavior, and the composite internalizing and externalizing scores were seen only in conjunction with high PAH exposure. Fewer significant effects with weaker effect sizes were observed in the low-PAH-exposure group. Maternal demoralization during pregnancy appears to have a greater effect on child neurobehavioral development among children who experienced high prenatal PAH exposure. The results provide the first evidence of an interaction between prenatal exposure to maternal demoralization and air pollution on child neurobehavioral development, indicating the need for a multifaceted approach to the prevention of developmental problems in children.

Neighborhood Social Context and Individual Polycyclic Aromatic Hydrocarbon Exposures Associated with Child Cognitive Test Scores.

Childhood cognitive and test-taking abilities have long-term implications for educational achievement and health, and may be influenced by household environmental exposures and neighborhood contexts. This study evaluates whether age 5 scores on the Wechsler Preschool and Primary Scale of Intelligence-Revised (WPPSI-R, administered in English) are associated with polycyclic aromatic hydrocarbon (PAH) exposure and neighborhood context variables including poverty, low educational attainment, low English language proficiency, and inadequate plumbing. The Columbia Center for Children's Environmental Health enrolled African-American and Dominican-American New York City women during pregnancy, and conducted follow-up for subsequent childhood health outcomes including cognitive test scores. Individual outcomes were linked to data characterizing 1-km network buffers around prenatal addresses, home observations, interviews, and prenatal PAH exposure data from personal air monitors. Prenatal PAH exposure above the median predicted 3.5 point lower total WPPSI-R scores and 3.9 point lower verbal scores; the association was similar in magnitude across models with adjustments for neighborhood characteristics. Neighborhood-level low English proficiency was independently associated with 2.3 point lower mean total WPPSI-R score, 1.2 point lower verbal score, and 2.7 point lower performance score per standard deviation. Low neighborhood-level educational attainment was also associated with 2.0 point lower performance scores. In models examining effect modification, neighborhood associations were similar or diminished among the high PAH exposure group, as compared with the low PAH exposure group. Early life exposure to personal PAH exposure or selected neighborhood-level social contexts may predict lower cognitive test scores. However, these results may reflect limited geographic exposure variation and limited generalizability.

Abstract 2643: Interactions between polycyclic aromatic hydrocarbon exposure and genetic polymorphisms on benzo(a)pyrene-DNA adducts in a Polish cohort of mothers and newborns

Abstract 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 single nucleotide polymorphism (SNP) frequency in genes related to PAH metabolism and detoxification, and explored the interactions between PAH exposure and SNPs 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 Polish mothers and newborns in Krakow, Poland. WBC DNA was isolated from cord blood, and genetic polymorphisms and BaP-DNA cord adducts were then measured in 503 mothers and 445 newborns. Maternal PAH exposure was measured during pregnancy with a personal air exposure monitor. For this study 7 maternal and newborn genes related to PAH metabolism, detoxification and repair were selected for SNP analyses: CYP1A1, CYP1A2, CYP1B1, GSTM3, GSTT2, NQO1 and XRCC1. SNP x PAH interactions on logarithmic (ln)-transformed BaP-DNA adduct levels were explored. Results We observed a number of significant interactions between high PAH exposure and SNPs in both mothers and newborns on BaP-DNA adducts in cord blood. For example, the interaction between a CYP1A2 SNP (rs2069514) and high PAH exposure on cord BaP-DNA adducts in newborns was significant (α=−1.34, p<0.01). We will present significant interaction results from analyses performed on both maternal and newborn CYP1A1, CYP1A2, GSTM3, GSTT2, NQO1 and XRCC1 SNPs. Discussion It is biologically plausible that an individual's abilities to metabolically activate and detoxify BaP and repair DNA damage play a role in susceptibility to DNA adduct formation following prenatal PAH exposure. Ultimately, this susceptibility could correlate with future risk of cancer development. Our findings of several SNP x PAH exposure interactions on cord BaP-DNA adducts support 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 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2643. doi:1538-7445.AM2012-2643

High levels of 1-hydroxypyrene and hydroxyphenanthrenes in urine of children and adults from Afghanistan

Among a health cooperation project, we had the opportunity to study the internal polycyclic aromatic hydrocarbon (PAH) exposure of residents from urban and rural areas in Afghanistan. Urine samples from 13 children (age 2.0-9 years) and 42 adults (age 20-65 years) were collected. A total of 25 participants were from Kabul, and 30 participants lived in a rural area. The determination of 1-hydroxypyrene and hydroxyphenanthrenes was carried out by high performance liquid chromatography and fluorescence detection. Median (range) were as follows (n=55): 1-hydroxypyrene 1646 ng/l (71-16,288 ng/l) and sum of 1-, 2- and 9-, 3-, 4-OH-phenanthrenes 3602 ng/l (116-19,670 ng/l). These results indicate a high PAH exposure, compared with the general population in more developed countries. The levels of 1-hydroxypyrene in urine of women (all non-smokers) from the rural area were higher than those from Kabul (N, median, range): rural 15, 2095, 334-11,357 ng/l; Kabul 11, 748,137-5332 ng/l. All households from the rural area used open fires for cooking and energy. We conclude that populations in low-developed countries may be at special risk to increased PAH exposure due to inadequate control of air pollution from car emissions and due to burning of biomass fuels for cooking and household energy.

Abstract 2753: Interactions between PAH exposure and genetic polymorphisms on BaP-DNA adducts in a NYC cohort of African American and Dominican mothers and newborns

Abstract 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

Exposure to polycyclic aromatic hydrocarbons and missed abortion in early pregnancy in a Chinese population

Background Polycyclic aromatic hydrocarbons (PAHs) are formed during incomplete burning of fossil fuels, wood, and tobacco products. High PAH exposure has been associated with low birth weight, intrauterine growth restriction, and preterm birth, but little is known about its impact on adverse outcomes in early pregnancy such as in-utero fetal death. Objectives To examine associations between exposure to PAHs and missed abortion in which the embryo has died but a miscarriage has not yet occurred during early pregnancy in a Chinese population in Tianjin. Methods A case–control study was conducted from April to November, 2007 in Tianjin, China. Cases experienced a missed abortion while controls underwent elective abortions before 14 weeks of pregnancy. Eighty-one cases were recruited from four hospitals, with the same number of controls matched on hospital, maternal age (± 8 years), gravidity (1 or >1), and gestational age (± 30 days). Two maternal measures of PAH exposures were obtained based on benzo[ a]pyrene (BaP) DNA adducts in 1) aborted tissues and 2) maternal blood (for a subset of subjects). In addition, proxy measures for PAH exposures from different sources were derived from maternal interviews. Results In conditional logistic regression analyses, we estimated more than 4-fold increase in risk of having experienced a missed abortion in women with above the median levels of blood BaP-DNA adducts (adjusted OR = 4.27; 95% CI, 1.41–12.99); but no increase with adduct levels in aborted tissues (adjusted OR = 0.76; 95% CI, 0.37–1.54). BaP-DNA adduct levels in maternal blood and aborted tissues were poorly correlated ( r = − 0.12; n = 102). Missed abortion risk also was higher among women reporting traffic congestion near the residence, commuting by walking, and performing regular cooking activities during pregnancy. Conclusion High levels of maternal PAH exposures may contribute to an increased risk of experiencing a missed abortion during early pregnancy.

CHILDREN’S HEALTH: Methylation Links Prenatal PAH Exposure to Asthma

CHILDREN’S HEALTH: Methylation Links Prenatal PAH Exposure to Asthma

Urinary naphthalene and phenanthrene as biomarkers of occupational exposure to polycyclic aromatic hydrocarbons

Objectives: The study investigated the utility of unmetabolised naphthalene (Nap) and phenanthrene (Phe) in urine as surrogates for exposures to mixtures of polycyclic aromatic hydrocarbons (PAHs). Methods: The report included...

Abstract B45: Prenatal exposure to polycyclic aromatic hydrocarbons (PAH), PAH-DNA adducts and genomic DNA methylation in cord blood

Abstract 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.

Higher urine 1-hydroxy pyrene glucuronide (1-OHPG) is associated with tobacco smoke exposure and drinking maté in healthy subjects from Rio Grande do Sul, Brazil

BackgroundThe highest rates of esophageal squamous cell carcinoma (ESCC) in Brazil occur in Rio Grande do Sul, the most southern state, which has incidence rates of 20.4/100,000/year for men and 6.5/100,000/year for women. Exposure to carcinogenic polycyclic aromatic hydrocarbons (PAHs) through tobacco smoke and other sources may increase the risk of ESCC. The aims of the current study were to investigate the degree and sources of PAH exposure of the inhabitants of this region of southern Brazil.MethodsTwo hundred healthy adults (half smokers, half non smokers, half male and half female) were recruited, given a standardized questionnaire, and asked to provide a urine sample for measurement of 1-hydroxypyrene glucuronide (1-OHPG), a PAH metabolite). Urine 1-OHPG concentrations were measured using immunoaffinity chromatography and synchronous fluorescence spectroscopy and urine cotinine was measured using a dipstick test. We examined factors associated with 1-OHPG concentration using Wilcoxon tests and multiple linear regression.ResultsUrine 1-hydroxypyrene glucuronide (1-OHPG) was successfully measured on 199 subjects. The median (interquartile range) of urine 1-OHPG in the 199 participants was 2.09 pmol/mL (0.51, 5.84). Tobacco smoke exposure and maté drinking were statistically significantly associated with higher urine 1-OHPG concentrations in the multivariate linear regression model.ConclusionTobacco smoke and maté both contribute to high levels of benzo[a]pyrene exposure in the people of southern Brazil. This high PAH exposure may contribute to the high rates of ESCC observed in this population. The increased urine 1-OHPG concentrations associated with maté suggest that contaminants, not just thermal injury, may help explain the increased risk of ESCC previously reported for maté consumption.

Determination of Anti-Bpde-DNA Adducts in Pah-Exposed Humans using the HPLC/Fluorescence Technique

In the present study, HPLC/fluorescence was applied to determine anti (±)-r-7, t-8-dihydroxy-t-9, 10-oxy-7,8,9,10-tetrahydrobenzo[a]pyrene (anti-BPDE)-DNA adducts formed in lymphocytes plus monocytes (LMF) from humans exposed to polycyclic aromatic hydrocarbons (PAH). Subjects were: 10 psoriatic patients (3 days after clinical coal tar (CT) treatment), 15 coke oven workers, 19 chimney sweeps, 35 aluminum anode plant workers, and 10 control subjects. Chronic and high PAH exposure in coke oven workers significantly increased the levels of BPDE-DNA adducts and the highest levels were seen in samples from smokers. Skin-acute (or short-term) and high PAH exposure of psoriatic patients do not increase DNA adduct levels. Determination of anti-BPDE-DNA adducts by means of this method is very promising for its sensitivity, specificity and simplicity and it may be applied in DNA adduct measurements to assesss high chronic PAH exposure and that it is thus suitable for industrial health purposes.

HPLC/fluorescence determination of anti-BPDE-DNA adducts in mononuclear white blood cells from PAH-exposed humans.

The aim of this study was to compare (+/-)-r-7,t-8-dihydroxy-t-9,10-oxy-7,8,9,10-tetrahydrobenzo[a]pyrene (anti-BPDE)-DNA adduct levels in groups of humans subjected to various levels of polycyclic aromatic hydrocarbon (PAH) (benzo[a]pyrene) exposure. An HPLC/fluorescence method was applied to detect specifically anti-BPDE-DNA adducts in mononuclear white blood cells [lymphocyte plus monocyte fraction (LMF)] from humans exposed to PAHs. A total of 130 subjects comprised the sample population: 26 psoriatic patients (3 days after clinical coal tar treatment of the skin), 15 coke oven workers, 19 chimney sweeps, 36 aluminium anode plant workers and 34 non-occupationally PAH-exposed subjects (controls). PAH exposure was assessed in each group by means of the urinary excretion of 1-pyrenol (mean group levels: 1.2, 0.7, 0.3, 65.0 and 0.1 micromol/mol creatinine in coke oven workers, chimney sweeps, aluminium plant anode workers, psoriatic patients and non-occupationally PAH-exposed subjects, respectively). HPLC/fluorescence analysis of BPDE-DNA adducts showed that the percentage of subjects with adduct levels exceeding the 95 percentile control subject value (8.9 adducts/10(8) nucleotides) was significantly high in coke oven workers (46.7%) and chimney sweeps (21.0%) (chi2 test, P < 0.01 and P < 0.05, respectively) but not in aluminium plant workers (11.1%) and psoriatic patients (0%). The increase in BPDE-DNA adduct levels in LMF (Ln values) was significantly related to chronic inhalatory and high PAH exposure (linear multiple regression analysis, F = 6.37, P < 0.01; t = 4.2, P < 0.001). Skin acute (or short-term) and high PAH exposure, charcoal-grilled meat consumption and smoking habit did not seem to influence BPDE-DNA adduct formation in LMF.

DNA damage in humans exposed to environmental and dietary polycyclic aromatic hydrocarbons

The paper describes recent research on human DNA damage related to environmental and dietary polycyclic aromatic hydrocarbon (PAH) exposures. The study populations either represent general populations of large geographical regions, or their exposure situation may have relevance to the general population. In Silesia, Poland, and Northern Bohemia, Czech Republic, where coal-based industry and domestic heating are the major sources of PAHs, significant differences have been observed in white blood cell DNA adducts and cytogenetic biomarkers between environmentally exposed and rural control populations, and significant seasonal variations of DNA damage have been detected. Bus drivers, traffic policemen and local residents have been involved in biomarker studies in Copenhagen, Athens, Genoa and Cairo, and differences have been measured in the level of DNA damage of urban and rural populations. Burning of smoky coal in unvented homes in Xuan Wei region, China, causes high PAH exposure of residents, which has been reflected in DNA adduct levels in different tissues. Indoor wood burning in open fireplaces did not increase human DNA adduct levels. Oil-well fires left burning in Kuwait after the Persian Gulf war created an unprecedented environmental pollution. However, insignificant environmental PAH levels were measured several miles from these fires. Aromatic and PAH-DNA adduct levels in white blood cells of US Army soldiers were lower during their deployment in Kuwait, than in Fulda, Germany, where they were stationed before and after serving in Kuwait. The contribution of dietary PAH exposure to blood cell DNA adduct levels had been demonstrated in studies in which volunteers consumed heavily charbroiled beef. Environmental tobacco smoke did not cause detectable changes, as measured by 32 P-postlabelling , in DNA adduct levels in non-smokers. In the reviewed studies, observed DNA adduct levels were generally in the range of 1 to 10 adducts, and not higher than 40 adducts in 10 8 nucleotides. Typically, 1.5 to 3-fold differences have been detected in DNA adduct levels between the exposed and control groups.

97/00227 Liquid chromatographic separation of isomeric mono-aromatic ring hydrocarbons in coal-derived oils by carbon packed column

The paper describes recent research on human DNA damage related to environmental and dietary polycyclic aromatic hydrocarbon (PAH) exposures. The study populations either represent general populations of large geographical regions, or their exposure situation may have relevance to the general population. In Silesia, Poland, and Northern Bohemia, Czech Republic, where coal-based industry and domestic heating are the major sources of PAHs, significant differences have been observed in white blood cell DNA adducts and cytogenetic biomarkers between environmentally exposed and rural control populations, and significant seasonal variations of DNA damage have been detected. Bus drivers, traffic policemen and local residents have been involved in biomarker studies in Copenhagen, Athens, Genoa and Cairo, and differences have been measured in the level of DNA damage of urban and rural populations. Burning of smoky coal in unvented homes in Xuan Wei region, China, causes high PAH exposure of residents, which has been reflected in DNA adduct levels in different tissues. Indoor wood burning in open fireplaces did not increase human DNA adduct levels. Oil-well fires left burning in Kuwait after the Persian Gulf war created an unprecedented environmental pollution. However, insignificant environmental PAH levels were measured several miles from these fires. Aromatic and PAH-DNA adduct levels in white blood cells of US Army soldiers were lower during their deployment in Kuwait, than in Fulda, Germany, where they were stationed before and after serving in Kuwait. The contribution of dietary PAH exposure to blood cell DNA adduct levels had been demonstrated in studies in which volunteers consumed heavily charbroiled beef. Environmental tobacco smoke did not cause detectable changes, as measured by 32P-postlabelling, in DNA adduct levels in non-smokers. In the reviewed studies, observed DNA adduct levels were generally in the range of 1 to 10 adducts, and not higher than 40 adducts in 108 nucleotides. Typically, 1.5 to 3-fold differences have been detected in DNA adduct levels between the exposed and control groups.