Benzo-a-Pyrene: Environmental Partitioning and Human Exposure

Hattemer‐Frey, Holly A.; Travis, Curtis C.

doi:10.1177/074823379100700303

Cited by 203 publications

(89 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast, nonmeat items contained up to 0.5 ng/g [Kazerouni et al, 2001]. The daily dietary intake of B[a]P has been estimated to range from 120 to 2800 ng/day [Hattemer-Frey et al, 1991], with average values approximating 600 ng/day [Scherer et al, 2000]. Catabolism of PAHs can generate reactive diol-epoxides, which have been shown to form stable DNA adducts at mutational hotspots in the p53 and Harvey-ras genes, disrupt transcription, and the binding affinity of Sp1 and E2F transcription heterodimers to DNA [MacLeod et al, 1995;Denissenko et al, 1996;Butler et al, 1997].…”

Section: Pahs As Exogenous Risk Factors In Carcinogenesismentioning

confidence: 99%

Epigenetics of breast cancer: Polycyclic aromatic hydrocarbons as risk factors

Jeffy

Chirnomas

Romagnolo

2002

Environ and Mol Mutagen

View full text Add to dashboard Cite

In the absence of a causal relationship between the incidence of sporadic breast cancer and occurrence of mutations in breast cancer susceptibility genes, efforts directed to investigating the contribution of environmental xenobiotics in the etiology of sporadic mammary neoplasia are warranted. Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous pollutants, which have been shown to induce DNA damage and disrupt cell cycle progression. In this report we discuss published data pointing to PAHs as a risk factor in carcinogenesis, and present findings generated in our laboratory suggesting that the mammary tumorigenicity of PAHs may be attributable, at least in part, to disruption of BRCA-1 expression by reactive PAHmetabolites. We report that benzo[a]pyrene (B[a]P), selected as a prototype PAH, disrupts BRCA-1 transcription in estrogen receptor (ER)-positive but not ER-negative breast cancer cells. The reduced potential for BRCA-1 expression in B[a]Ptreated cells coincides with disruption of cell cycle kinetics and accumulation of p53. These effects are counteracted by the AhR-antagonist ␣-naphthoflavone (ANF), and in breast cancer cells expressing mutant p53 or the E6 human papilloma virus protein. We suggest that exposure to PAHs may be a predisposing factor in the etiology of sporadic breast cancer by disrupting the expression of BRCA-1. Environ. Mol. Mutagen. 39:235-244, 2002.

show abstract

Section: Pahs As Exogenous Risk Factors In Carcinogenesismentioning

confidence: 99%

Epigenetics of breast cancer: Polycyclic aromatic hydrocarbons as risk factors

Jeffy

Chirnomas

Romagnolo

2002

Environ and Mol Mutagen

View full text Add to dashboard Cite

show abstract

“…Population studies detected the accumulation of TCDD in breast milk (13,14), suggesting that this agent may reach breast tissue and be a risk factor in mammary neoplasia. Another class of environmental pollutants is polycyclic aromatic hydrocarbons (PAH), including the prototypical carcinogen benzo(a)pyrene [B(a)P], which is found in cigarette smoke and cooked meat (15). Diet contributes average values of 600 ng/d of B(a)P (16).…”

Section: Introductionmentioning

confidence: 99%

The Ligand Status of the Aromatic Hydrocarbon Receptor Modulates Transcriptional Activation of BRCA-1 Promoter by Estrogen

Hockings¹,

Thorne²,

Kemp³

et al. 2006

Cancer Research

View full text Add to dashboard Cite

In sporadic breast cancers, BRCA-1 expression is downregulated in the absence of mutations in the BRCA-1 gene. This suggests that disruption of BRCA-1 expression may contribute to the onset of mammary tumors. Environmental contaminants found in industrial pollution, tobacco smoke, and cooked foods include benzo(a)pyrene [B(a)P] and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), which have been shown to act as endocrine disruptors and tumor promoters. In previous studies, we documented that estrogen (E2) induced BRCA-1 transcription through the recruitment of an activator protein-1/estrogen receptor-A (ERA) complex to the proximal BRCA-1 promoter. Here, we report that activation of BRCA-1 transcription by E2 requires occupancy of the BRCA-1 promoter by the unliganded aromatic hydrocarbon receptor (AhR). The stimulatory effects of E2 on BRCA-1 transcription are counteracted by (a) cotreatment with the AhR antagonist 3V -methoxy-4V -nitroflavone; (b) transient expression in ERAnegative HeLa cells of ERA lacking the protein-binding domain for the AhR; and (c) mutation of two consensus xenobiotic-responsive elements (XRE, 5V -GCGTG-3V ) located upstream of the ERA-binding region. These results suggest that the physical interaction between the unliganded AhR and the liganded ERA plays a positive role in E2-dependent activation of BRCA-1 transcription. Conversely, we show that the AhR ligands B(a)P and TCDD abrogate E2-induced BRCA-1 promoter activity. The repressive effects of TCDD are paralleled by increased recruitment of the liganded AhR and HDAC1, reduced occupancy by p300, SRC-1, and diminished acetylation of H4 at the BRCA-1 promoter region flanking the XREs. We propose that the ligand status of the AhR modulates activation of the BRCA-1 promoter by estrogen. (Cancer Res 2006; 66(4): 2224-32)

show abstract

“…Previous work has shown that vegetation can accumulate both gas-phase and particle bound SVOCs from the atmosphere providing a means for air pollutants to enter the foodchain (Hattemer-Frey and Travis, 1991;Jones et al, 1991;EPA, 1994;McLachlan, 1996;Welsch-Pausch and McLachlan, 1998;EPA, 1998d;Bohme et al, 1999;Kaupp et al, 2000). Plants also accumulate pollutants from the soil but the importance of the soil-to-plant pathway for atmospheric pollutants is generally negligible (Welsch-Pausch et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

Contribution of locally grown foods in cumulative exposure assessments

Lobscheid

Maddalena

McKone

2004

J Expo Sci Environ Epidemiol

View full text Add to dashboard Cite

ABSTRACT:Both laboratory and field studies confirm the importance of vegetation for scavenging semi-volatile organic chemicals (SVOCs) from the atmosphere and a number of exposure studies have found that the dietary pathway is often a significant contributor to cumulative exposure for these chemicals. Exposure calculations based on published concentration data for foods indicate that the potential intake through ingestion is up to 1000 times that of inhalation for several persistent SVOCs. However, little information exists on the source-to-dietary intake linkage for SVOC's. Because of higher SVOC emissions to urban regions, this linkage is particularly important for foods that are grown, distributed and consumed in or near urban regions. The food pathway can also contribute to dietary exposure for populations that are remote from a pollutant source if the pollutants can migrate to agricultural regions and subsequently to the agricultural commodities distributed to that population. We use the characteristic travel distance (CTD) and available data within the CalTOX multimedia model framework to assess the contribution of local food markets to the fraction of cumulative food intake that is attributable to local sources. For a set of three representative multimedia SVOCsbenzo(a)pyrene, fluoranthene, and 2,3,7,8-TCDD, we explore the contribution of airborne SVOC's to cumulative uptake through the local food consumption pathway. We use the population based intake fraction (iF) to determine how SVOC intake varies among food commodities and compares to inhalation. The approach presented here provides a useful framework and starting point for source-to-intake assessments for the air-to-dietary exposure pathway. p 2 of 41

show abstract

Benzo-a-Pyrene: Environmental Partitioning and Human Exposure

Cited by 203 publications

References 36 publications

Epigenetics of breast cancer: Polycyclic aromatic hydrocarbons as risk factors

Epigenetics of breast cancer: Polycyclic aromatic hydrocarbons as risk factors

The Ligand Status of the Aromatic Hydrocarbon Receptor Modulates Transcriptional Activation of BRCA-1 Promoter by Estrogen

Contribution of locally grown foods in cumulative exposure assessments

Contact Info

Product

Resources

About