Evidence map›Paper›PMID 29204680›Full record

ArticleArchives of toxicology2018

Association between polymorphism of GSTP1, GSTT1, GSTM1 and CYP2E1 genes and susceptibility to benzene-induced hematotoxicity.

Mohamad Amin Nourozi, Masoud Neghab, Javad Tavakkoly Bazzaz, Saharnaz Nejat, Yaser Mansoori, Seyed Jamaleddin Shahtaheri

Open access · hybridAbstract read
In one paragraph

Article in Archives of toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 29% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 31 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Mohamad Amin NouroziDepartment of Occupational Health Engineering, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Masoud NeghabDepartment of Occupational Health Engineering, Research Center for Health Sciences, Institute of Health, School of Health, Shiraz University of Medical Sciences, Shiraz, Iran.
Javad Tavakkoly BazzazDepartment of Medical Genetics, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Saharnaz NejatDepartment of Epidemiology and Biostatistics, School of Public Health, Knowledge Utilization Research Center (KURC), Tehran University of Medical Sciences, Tehran, Iran.
Yaser MansooriNon-communicable Diseases Research Center, Fasa University of Medical Sciences, Fasa, Iran.
Seyed Jamaleddin ShahtaheriDepartment of Occupational Health Engineering, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. shahtaheri@tums.ac.ir.
Tehran University of Medical Sciences · IRFasa University of Medical Sciences · IRShiraz University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Occupational exposure to benzene has been associated with leukemia, anemia, leukopenia, and thrombocytopenia. Genetic susceptibility to benzene toxicity in humans may be related to variations in benzene metabolizing genes. The main objective of this study was to ascertain whether polymorphism of GSTP1, GSTM1, GSTT1 and CYP2E1 genes might influence susceptibility to the adverse effects of benzene among employees of a petrochemical plant. In this cross-sectional study, 124 employees of a petrochemical plant who had been occupationally exposed to benzene and had one or more abnormal hematological parameter (cases) and 184 subjects with a similar exposure scenario, free from any abnormal hematological parameters (referent) were studied. Atmospheric concentrations of benzene were measured and GSTM1 and GSTT1 genotypes were evaluated using the multiplex polymerase chain reaction (PCR) technique. Additionally, GSTP1 and CYP2E1 genotypes were determined by PCR- restriction fragment length polymorphism (PCR-RFLP). The frequency of null GSTT1 genotype in cases was significantly higher than that of referent group (32.3 vs. 18.5%, OR 2.1, 95% CI 1.23-3.56, p = 0.004). The mean value of platelets in subjects with null GSTT1 genotype was significantly lower than that of individuals with positive GSTT1 genotype (p = 0.015). Conversely, the mean value of leukocytes was significantly higher in subjects with null GSTM1 genotype as compared to those with positive GSTM1 genotype (p = 0.026). Logistic regression analysis showed that, subjects with null GSTT1 genotype had a significantly higher risk for hematological disorders, as compared to those with positive GSTT1 genotype (OR 2.1, 95% CI 1.23-3.56). Moreover, subjects with both null GSTT1 and GSTM1 genotypes had a significantly higher risk for hematological disorders as compared to subjects with positive GSTT1 and GSTM1 genotypes (OR 2.35, 95% CI 1.14-4.8). The results of this study showed that, individuals carrying null GSTT1 or both null STT1 and GSTM1 genotypes had a higher risk and were more susceptible to benzene-induced hematological disorders.

Indexed as

Genetic Predisposition to DiseasePolymorphism, Restriction Fragment LengthAdultAir Pollutants, OccupationalBenzeneCross-Sectional StudiesCytochrome P450 Family 2ErythrocytesGlutathione S-Transferase piGlutathione TransferaseHematologic DiseasesHemoglobinsHumansIranLeukocytesLogistic ModelsAir Pollutants, OccupationalBenzeneCYP2F1 protein, humanCytochrome P450 Family 2Glutathione S-Transferase piglutathione S-transferase T1Glutathione TransferaseGSTP1 protein, humanHemoglobinsGenetic polymorphismPetrochemical employeesSusceptibility to benzene-induced hematotoxicity

Identifiers

PMID29204680
PMCPMC6002464
OpenAlexW2771650437

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.