Biomarkers of carcinogen exposure and cancer risk in a coke plant.

Assennato, Giorgio; Ferri, Giovanni Maria; Tockman, M. S.; Poirier, Miriam C.; Schoket, Bernadette; Porro, Antônio; Corrado, Vincenzo; Strickland, Paul T.

doi:10.1289/ehp.9399237

Cited by 7 publications

(1 citation statement)

References 10 publications

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“…The risk of gastric cancer and nonmalignant respiratory diseases in workers in the coke shipment department was increased. Similarly, to evaluate the association between a carcinogenic exposure indicator (IPA adducts to peripheral blood leukocyte DNA) and an early indicator of neoplastic transformation (antigens of the epithelial cell membrane of sputum cells), Assennato et al [88] recruited 350 coke oven workers and 100 unexposed workers. The results showed that smokers, people with reduced lung function, and those with morphological dysplasia of sputum cells had high levels of DNA adducts; however, no significant difference was found between the groups of coke oven workers and unexposed controls.…”

Section: Relationship Between Different Biomarkers and Vital Statusmentioning

confidence: 99%

Environmental Monitoring of PAHs Exposure, Biomarkers and Vital Status in Coke Oven Workers

Vimercati

Bisceglia

Cavone

et al. 2020

IJERPH

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A follow-up study of a cohort of workers from a coke plant compared with a control group from the same industrial area was conducted in 2019. The recruitment and environmental and biomarker measurements were performed during 1993/1994. The environmental concentrations of polycyclic aromatic hydrocarbons (PAH), B(a)P, pyrene and nitro-PAH were measured. Personal data were collected via an individual semi-structured questionnaire by a trained physician. All biomarkers were measured after a specific blood drawing for every test. Significant risks (ORs) were observed for nitro-PAH (≥0.12 µg/m3) [OR = 7.96 (1.01–62.82)], urinary 1-hydroxypyrene (1-OHpy) (≥0.99 µmoles/moles of creatinine) [OR = 11.71 (1.47–92.90)], PAH DNA adducts (P32) (≥2.69 adducts/108 nucleotides) [OR = 5.46 (1.17–25.58)], total nitro-PAH hemoglobin adducts (≥161.68 fg/µg of Hb) [OR = 5.92 (1.26–27.86)], sister chromatid exchange (SCE) with TCR (≥377.84 SCE/cell chromosomes) [OR = 13.06 (3.95–93.10)], sister chromatid exchange with T (≥394.72 total SCE) [OR = 13.06 (3.95–93.10)], and sister chromatid exchange with X (≥8.19 mean SCE) [OR = 13.06 (3.95–93.10)]. Significant risk of death for all causes and chromosomal aberrations (48 h) (OR = 7.19 [1.19–43.44]) or micronuclei in culture at 48 h (OR = 3.86 [1.04–14.38]) were also found.

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Section: Relationship Between Different Biomarkers and Vital Statusmentioning

confidence: 99%

Environmental Monitoring of PAHs Exposure, Biomarkers and Vital Status in Coke Oven Workers

Vimercati

Bisceglia

Cavone

et al. 2020

IJERPH

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Chlorophyllin significantly reduces benzo[a]pyrene‐DNA adduct formation and alters cytochrome P450 1A1 and 1B1 expression and EROD activity in normal human mammary epithelial cells

Keshava

Divi

Einem

et al. 2009

Environ and Mol Mutagen

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We hypothesized that chlorophyllin (CHLN) would reduce BP-DNA adduct levels. Using NHMECs exposed to 4 μM BP for 24 hr in the presence or absence of 5 μM CHLN, we measured BP-DNA adducts by chemiluminescence immunoassay (CIA). The protocol included the following experimental groups: BP alone, BP given simultaneously with CHLN (BP+CHLN) for 24 hr, CHLN given for 24 hr followed by BP for 24 hr (preCHLN, postBP), and CHLN given for 48 hr with BP added for the last 24 hr (preCHLN, postBP+CHLN). Incubation with CHLN decreased BPdG levels in all groups, with 87 % inhibition in the preCHLN, postBP+CHLN group. To examine metabolic mechanisms, we monitored expression by Affymetrix microarray (U133A), and found BP-induced up-regulation of CYP1A1 and CYP1B1 expression, as well as up-regulation of groups of interferoninducible, inflammation and signal transduction genes. Incubation of cells with CHLN and BP in any combination decreased expression of many of these genes. Using real time PCR (RT-PCR) the maximal inhibition of BP-induced gene expression, >85% for CYP1A1 and >70% for CYP1B1, was observed in the preCHLN, postBP+CHLN group. To explore the relationship between transcription and enzyme activity, the ethoxyresorufin-O-deethylase (EROD) assay was used to measure the combined CYP1A1 and CYP1B1 activities. BP exposure caused the EROD levels to double, compared to the unexposed controls. The CHLN-exposed groups all showed EROD levels similar to the unexposed controls. Therefore, the addition of CHLN to BP-exposed cells reduced BPdG formation and CYP1A1 and CYP1B1 expression, but EROD activity was not significantly reduced.

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The influence of cytochrome P450 1A1 and glutathione S-transferase M1 genotypes on biomarker levels in coke-oven workers

Brescia¹,

Celotti

Clonfero

et al. 1999

Archives of Toxicology

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The present study has the aim of evaluating gene-environment interaction on the levels of different biomarkers in coke-oven workers exposed to PAH. In order to assess whether the levels of some biomarkers (PAH-DNA adducts, nitro-PAH adducts to Hb and MN frequency) could be modulated by the genetic metabolic polymorphisms for CYP1A1 and GSTM1, we analysed in 76 coke-oven workers and 18 controls the CYP1A1 (MspI and Ile/Val sites) and the GSTM1 genotypes by a PCR assay. In individuals with shared setup of CYP1A1 or GSTM1 genotypes, we analysed how the specified biomarkers correlated with total PAH exposure (urinary levels of 1-hydroxypyrene) both by a stratified analysis and logistic regression modelling. Statistically significant (P = 0.03 and P = 0.01) higher percentages of the more susceptible GSTM1- subjects compared to the GSTM1+ subjects and of the more susceptible CYP1A1 Ile/Val individuals compared to the CYP1A1 Ile/Ile individuals were detected for high levels of PAH-DNA adducts in the high exposure group (namely high levels of 1-OHP). A statistically significant association was observed between increased PAH-DNA adduct levels and the more susceptible GSTM1- genotype (P.O.R. = 4.18, P = 0.03) in a logistic regression modelling and a significant interaction between PAH exposure and GSTM1-genotype was found for PAH-DNA adducts. No effect of these metabolic genotypes was observed for MN frequency and nitro-PAH adducts to Hb. In conclusion, a gene-environment interaction between PAH exposure and two metabolic genotypes involved in activation (CYP1A1) and detoxification (GSTM1) of PAHs, respectively, has been identified.

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Biomarkers of carcinogen exposure and cancer risk in a coke plant.

Cited by 7 publications

References 10 publications

Environmental Monitoring of PAHs Exposure, Biomarkers and Vital Status in Coke Oven Workers

Environmental Monitoring of PAHs Exposure, Biomarkers and Vital Status in Coke Oven Workers

Chlorophyllin significantly reduces benzo[a]pyrene‐DNA adduct formation and alters cytochrome P450 1A1 and 1B1 expression and EROD activity in normal human mammary epithelial cells

The influence of cytochrome P450 1A1 and glutathione S-transferase M1 genotypes on biomarker levels in coke-oven workers

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