[A study on the inherited susceptibility of chromosomal damage in peripheral blood lymphocytes among coke oven workers].
OBJECTIVE
To investigate the association between polymorphisms of metabolic enzyme genes and chromosomal damage risk in peripheral blood lymphocytes among coke oven workers.


METHODS
One hundred and fourty-nine coke oven workers and 24 referents without occupational polycyclic aromatic hydrocarbons (PAH) exposure were recruited in this study. Urinary 1-hydroxypyrene levels were measured as the internal dose of PAH exposure. The 6 per 1 000 of micronucleus value was used as the cut-off value to determine whether the individual's chromosomal damage was positive. The genotypes of CYP1A1, GSTM1, GSTT1, GSTP1, CYP2E1, NQO1, NAT2 and mEH genes were determined by PCR-based methods. Multiple logistic regression was used to calculate the adjusted ORs and the 95% CI for the risk of chromosomal damage and to analyze the gene-gene interaction.


RESULTS
In 173 subjects, after adjusting the occupational exposure, age, sex, smoking and drinking status, the subjects with GSTM1 null genotype have significantly higher risk for chromosomal damage than subjects with GSTM1 positive genotype (adjusted OR = 2.01, 95% CI = 1.03 -3.91). Compared with the wild homozygotes at P187S site of NQO1 gene, the variant homozygotes have significantly higher risk for chromosomal damage (adjusted OR = 3.18, 95% CI = 1.18 - 8.62). The subjects with variant allele at H113Y site of mEH gene have significantly lower risk for chromosomal damage (adjusted OR = 0.40, 95% CI = 0.19 - 0.88). No significant associations were found for other gene polymorphisms and chromosomal damage risk. In addition, the gene-gene interactions were also found among GSTM1, NQO1 gene P187S and mEH gene H113Y polymorphisms for the risk of chromosomal damage risk.


CONCLUSIONS
Significant associations between genetic polymorphisms in GSTM1, NQO1 and mEH gene and risk for chromosomal damage were found among occupational PAH-exposed workers, which related to the mechanism of PAH carcinogenesis.
Leng
Shu-guang
SG
National Institute for Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing 100050, China.
Zheng
Yu-xin
YX
Pan
Zu-fei
ZF
Niu
Yong
Y
Dai
Yu-fei
YF
Wang
Ya-wen
YW
Zhang
Wen-zhong
WZ
Xiao
Jun
J
Wang
Zhong-xu
ZX
Li
Tao
T
He
Feng-sheng
FS
D000328:Adult; D004249:DNA Damage / Q000235:genetics*; D004851:Epoxide Hydrolases / Q000235:genetics; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D005982:Glutathione Transferase / Q000235:genetics; D006801:Humans; D016015:Logistic Models; D008214:Lymphocytes / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D016660:NAD(P)H Dehydrogenase (Quinone) / Q000235:genetics; D016273:Occupational Exposure; D011084:Polycyclic Aromatic Hydrocarbons / Q000506:poisoning; D011110:Polymorphism, Genetic; D011721:Pyrenes / Q000032:analysis; D012307:Risk Factors
D004851:Epoxide Hydrolases; D005982:Glutathione Transferase; D016660:NAD(P)H Dehydrogenase (Quinone); D011084:Polycyclic Aromatic Hydrocarbons; D011721:Pyrenes; C447479:NQO1 protein, human; C033146:1-hydroxypyrene