Dermal exposure to polycyclic aromatic hydrocarbons in asphalt workers

Fustinoni, Silvia; Campo, Laura; Cirla, P E; Martinotti, I; Buratti, M; Longhi, Omar; Foà, V.; Bertazzi, Pier Alberto

doi:10.1136/oem.2009.050344

Cited by 32 publications

(22 citation statements)

References 40 publications

(28 reference statements)

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“…Therefore they are readily absorbed through biological membranes, and bioactivated through various metabolic pathways, converting the parent PAH to electrophilic metabolites, thus transforming inactive compounds into carcinogenic and mutagenic species (McClean et al, 2007; Fustinoni et al, 2010; Jacques et al, 2010; Crowell et al, 2011). Evidence of three separate pathways of PAH metabolism have been published in the scientific literature (reviewed in Wue and Warshawsky, 2005).…”

Section: Introductionmentioning

confidence: 99%

Cytochrome P450 1b1 in polycyclic aromatic hydrocarbon (PAH)-induced skin carcinogenesis: Tumorigenicity of individual PAHs and coal-tar extract, DNA adduction and expression of select genes in the Cyp1b1 knockout mouse

Siddens

Bunde

Harper

et al. 2015

Toxicology and Applied Pharmacology

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FVB/N mice wild-type, heterozygous or null for Cyp 1b1 were used in a two-stage skin tumor study comparing PAH, benzo[a]pyrene (BaP), dibenzo[def,p]chrysene (DBC), and coal tar extract (CTE, SRM 1597a). Following 20 weeks of promotion with TPA the Cyp 1b1 null mice, initiated with DBC, exhibited reductions in incidence, multiplicity, and progression. None of these effects were observed with BaP or CTE. The mechanism of Cyp 1b1-dependent alteration of DBC skin carcinogenesis was further investigated by determining expression of select genes in skin from DBC-treated mice 2, 4 and 8 h post-initiation. A significant reduction in levels of Cyp 1a1, Nqo1 at 8 h and Akr 1c14 mRNA was observed in Cyp 1b1 null (but not wt or het) mice, whereas no impact was observed in Gst a1, Nqo 1 at 2 and 4 h or Akr 1c19 at any time point. Cyp 1b1 mRNA was not elevated by DBC. The major covalent DNA adducts, dibenzo[def,p]chrysene-(±)-11,12-dihydrodiol-cis and trans-13,14-epoxide-deoxyadenosine (DBCDE-dA) were quantified by UHPLC-MS/MS 8 h post-initiation. Loss of Cyp1 b1 expression reduced DBCDE-dA adducts in skin but not to a statistically significant degree. The ratio of cis-to trans-DBCDE-dA adducts was higher in skin than other target tissues such as spleen, lung and liver (oral dosing). These results document that Cyp 1b1 plays a significant role in bioactivation and carcinogenesis of DBC in a two-stage mouse skin tumor model and that loss of Cyp 1b1 has little impact on tumor response with BaP or CTE as initiators.

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Section: Introductionmentioning

confidence: 99%

Cytochrome P450 1b1 in polycyclic aromatic hydrocarbon (PAH)-induced skin carcinogenesis: Tumorigenicity of individual PAHs and coal-tar extract, DNA adduction and expression of select genes in the Cyp1b1 knockout mouse

Siddens

Bunde

Harper

et al. 2015

Toxicology and Applied Pharmacology

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show abstract

“…In construction workers, the carcinogenic risk derives from both chronic dermal and airborne exposure. 2 …”

Section: Introductionmentioning

confidence: 99%

Using baby oil to remove asphalt from burn

Nawrocki

Thompson

2015

CJEM

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“…Formed during incomplete combustion of organic matter, B[a]P is released into the environment from municipal refuse, vehicle exhaust fumes [Courter et al, 2007;Agarwal, 2009], industrial processes and the manufacture of products such as coal, tar, asphalt, petroleum [ATSDR, 1995]. Human exposure to B[a]P may occur as a result of cigarette smoking [Adams et al, 1987;Duarte-Salles et al, 2010], consumption of contaminated foods or water Wretling et al, 2010] and occupational exposures [Boffetta et al, 1997;Bohlin et al, 2010;Fustinoni et al, 2010].…”

Section: Introductionmentioning

confidence: 99%