三氯乙烯药疹样皮炎个体易感性指标的研究

目的探索磺胺二甲嘧啶检测N-乙酰基转移酶2（NAT2）代谢分型作为三氯乙烯（TCE）药疹样皮炎的个体易感性指标,用于TCE接触劳动者上岗前职业健康检查禁忌证的筛选,减少TCE药疹样皮炎的发生概率。方法比较17例患者和52例健康TCE接触工人N-乙NAT2代谢型分布,并计算相对危险度;对NAT2慢代谢型劳动者进行行政干预,了解干预效果。结果NAT2代谢型在2组间的分布差异有统计学意义（P〈0．01）,且NAT2慢代谢型出现三氯乙烯药疹样皮炎的危险性比快代谢型高（OR=10．50;95％CI=2．644～41．695）。干预前后发病率差异有统计学意义（P〈0．05）。结论NAT2代谢分型可能是影响三氯乙烯药疹样皮炎个体易感性的重要原因,利用磺胺二甲嘧啶检测NAT2代谢分型可能可以用于三氯乙烯接触职业禁忌的筛查。     

NAT2,CYP2B6和GSTP1基因多态性与苯乙烯生物监测的关系

目的：探讨NAT2，CYP2B6和GSTP1基因多态性与苯乙烯生物监测之间的关系。方法：选择58名接触苯乙烯的工人为研究对象，应用PCR-RFLP法判定基因型；应用高效液相色谱法测定其尿中三种代谢产物（苯乙醇酸、苯乙醛酸和苯乙烯巯基尿酸）的含量；并分析NAT2，CYP2B6和GSTP1基因多态性对接触不同水平苯乙烯工人尿中代谢产物含量有无显著影响（P〈0.05）。结果：CYP2B6（BsrI）不同基因型苯乙烯尿中代谢产物含量有显著性差异；GSTP1（BsmAI）和NAT2 M3基因型在苯乙烯代谢中的作用差异均无统计学意义。结论：除传统生物检测指标如尿中化学代谢物和早期生物效应等，某些苯乙烯代谢酶基因多态性对其生物监测指标具有一定影响，因此也可作为遗传易感性生物标志物，用来评价苯乙烯接触人群的遗传易感性。     

MPO和NAT2基因多态性与成人急性白血病易感性

目的研究髓过氧化物酶（MPO）和N-乙酰基转移酶2（NAT2）基因多态性与成人急性白血病易感性的关系.方法用1∶1配对病例-对照研究方法,收集成人急性白血病患者和对照各139例,应用聚合酶链-内切酶片段（PCR-RFLP）方法分析病例组和对照组MPO和NAT2的基因多态性,比较不同基因型与成人急性白血病易感性.结果 MPO-463A等位基因分布频率病例组低于对照组,MPO（G-463A）各基因型在病例组与对照组中的分布差异有统计学意义（χ^2=7.026,P〈0.05,OR=0.505,95%CI=0.325～0.847）.NAT2乙酰化表型频率在病例组与对照组的分布差异无统计学意义（χ^2=2.260,P〉0.05）;但NAT2＊5 481T等位基因和NAT2＊6 590A等位基因分布频率病例组高于对照组（P〈0.05）.结论 MPO与成人急性白血病易感性相关,携带MPO（G-463A）突变基因型（GA/AA）个体可降低白血病的发病风险;NAT2乙酰化表型可能与白血病的易感性无关,但NAT2＊5（C481T）、NAT2＊6（G590A）单核苷酸突变频率病例组明显高于对照组.     

人类白细胞抗原DQ基因多态性与三氯乙烯药疹样皮炎易感性的关系

目的研究人类白细胞抗原DQ（HLA-DQ）基因多态性与三氯乙烯药疹样皮炎易感性的关系。方法应用聚合酶链反应产物直接测序方法,比较112例三氯乙烯药疹样皮炎病例和142例健康三氯乙烯接触工人HLA—DQA1和HLA—DQBl基因第2外显子氨基酸密码子多态性及等位基因型频率分布。结果病例组DQA1等位基因0201和060101／0602的分布频率[7．6％（17／224）和16．1％（36／224）]显著高于对照组[3．5％（10／284）和7．0％（20／284）],而病例组DQAl等位基因0103和050101／0503／0505的分布频率[5．8％（13／224）和8．9％（20／224）]显著低于对照组[10．9％（31／284）和17．3％（49／284）]。此外,病例组与对照组之间差异有统计学意义的氨基酸密码子多态性位点见于DQA1的5个密码子（25、41、52、54和69）。病例组与对照组HLA-DQB1等位基因的分布频率差异无统计学意义。结论HLA-DQA1基因多态性可能是导致三氯乙烯药疹样皮炎个体易感性差异的原因之一。     

醛、醇脱氢酶基因多态性与三氯乙烯药疹样皮炎易感性的关系

目的研究醛脱氢酶、醇脱氢酶基因多态性与三氯乙烯药疹样皮炎易感性的关系。方法应用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)方法,比较108例三氯乙烯药疹样皮炎病人和145例健康三氯乙烯接触工人醛脱氢酶2(ALDH2)、醇脱氢酶2(ADH2)和醇脱氢酶3(ADH3)的基因多态性分布,并计算相对危险度(OR)。结果ADH2和ADH3基因型分布在病人与接触对照工人中无显著性差异;ALDH2变异型基因(ALDH2*1/*2+ALDH2*2/*2)频率在病人中显著低于接触对照工人(分别为27·8%和43·4%,P=0·011),使三氯乙烯药疹样皮炎的危险性显著降低(OR=0·50,95%CI=0·29~0·85)。结论高活性ALDH2可能是导致三氯乙烯药疹样皮炎个体易感性差异的原因之一。     

山东地区NAT2基因多态性与乳腺癌易感性的研究

[目的]研究NAT2基因多态性与乳腺癌易感性的关系。[方法]采用1︰1配对病例-对照研究,对山东地区100例乳腺癌患者和100例健康对照者采用聚合酶链反应-限制性片段长度多态性分析(PCR-RFLP),检测NAT2基因多态性,分析NAT2基因多态性与乳腺癌易感性之间的关系。[结果]携带NAT2*5B等位基因者患乳腺癌危险性增加(OR=2.38,95%CI=1.54～3.67);慢基因型者患乳腺癌的危险性是快基因型者2.28倍(OR=2.28,95%CI=1.12～4.63);是中间基因型者2.14倍(OR=2.14,95%CI=1.08～4.24);慢型乙酰化患乳腺癌的危险性是快型乙酰化的2.11倍(OR=2.11,95%CI=1.15～3.88)。[结论]NAT2基因多态性在乳腺癌的遗传发病机制中起重要作用,携带NAT2*5B等位基因、慢基因型及慢型乙酰化能增加患乳腺癌的易感性。     

N-乙酰基转移酶基因多态性与肺癌易感性关系

目的探讨N-乙酰基转移酶基因2(NAT2)多态性与肺癌易感性关系。方法采用1∶1配对病例-对照研究,收集江苏省汉族人群原发性肺癌患者215例和相应非肿瘤对照215例。应用PCR-限制性片断长度多态性(RFLP)技术检测病例组与对照组NAT2基因M1、M2和M3等位基因突变频率,分析NAT2基因多态性与肺癌易感性之间的关系。结果M3等位基因频率在肺鳞癌组和对照组的分布差异有统计学意义(χ2=4.30,P<0.05),携带M3等位基因者患肺鳞癌危险性增加(OR=1.63,95%CI=1.03～2.59),尤其是增加不吸烟者患肺鳞癌的危险性(OR=2.23,95%CI=1.07～4.65)。未发现NAT2乙酰化基因型与肺癌发生有相关性。结论NAT2M3等位基因可能与不吸烟者肺鳞癌易感性有关。     

大肠癌代谢酶基因多态性的Meta分析

目的 综合评价代谢酶基因多态性与大肠癌危险性的关系。方法 应用Meta分析原理对国内42篇大肠癌相关代谢酶基因多态性的病例研究进行定量综合分析。统计处理采用M-H法或D-L法以及RevM4.1统计软件包。结果 GSTM1缺陷型，GSTT1缺陷型，GSTP1Llel105Val,NAT1*10,NAT2快速乙酰化表型/基因型，乙酰化表型，乙酰化基因型，CYP1A1MspI,CYP1A1Lle462Val,MTHFRC677T和MTRA2759G11个研究因素的综合统计量（OR值）分别为1.06,1.42,1.09,1.25,1.08,1.15,1.05,1.26,1.30,0.83和0.60。结论 GSTT1缺陷型，NAT2快速乙酰化表型/基因型和NAT2快速乙酰化表型可能与大肠癌的发生有关。     

毒物代谢酶基因多态性与胃癌易感性

简要综述毒物代谢酶一相酶细胞色素P4502E1（CYP4502E1）、二相酶谷胱甘肽S－转硫酶M1、T1GSTM1、GSTT1）、N－乙酰化转移酶（NAT）的基因多态性与胃癌的遗传易感性的国内外研究进展。     

代谢酶基因多态性与结直肠癌易感性关系的病例对照研究

目的以自然随访人群为研究对象，研究Ⅰ、Ⅱ相代谢酶基因多态性与结直肠癌（CRC）易感性的关系。方法采用聚合酶链反应（PCR）-限制性片段长度多态性（RFLP）、等位基因特异性PCR（AS-PCR）和多重PCR分析技术，检测140例CRC患者和343名健康对照细胞色素P450氧化酶CYP1A16235T／C、CYP1A2734C／A、CYP2E1—12596／C和-1019C／T各位点多态性，谷胱甘肽转移酶GSTMu（GSTM1）和GSTTheta（GSTT1）缺陷型，以及N-乙酰基转移酶基因NAT1和NAT2各等位基因型分布频率，分析其对CRC易感性的影响。结果等位基因CYP1A16235C、CYP1A2734A、CYP2E1—1259C、CyP2E1—1019T、GSTM1缺陷型、GSTT1缺陷型、NAT1＊10和NAT2Mx（x=1，2，3）的分布频率在病例组依次为31．65％、63．77％、23．02％、32．61％、57．25％、17．39％、26．45％和39．21％，对照组依次为39．85％、66．62％、20．27％、28．61％、55．46％、20．35％、25．22％和39．36％，所有基因型分布均符合Hardy—Weinberg平衡定律。单基因、多基因联合分层分析表明，CYP1A16235CC突变纯合型可显著降低CRC风险（OR=0．79，95％CI=0．63～0．99）；在携带CYP1A2734A等位基因个体，CYP1A16235C等位基因也可显著降低CRC风险（OR=0．53．95％CI：0．34～0．83）；在GSTT1缺陷型个体，GSTM1缺陷型可使机体罹患CRC的风险显著升高（OR=4．41，95％CI=1．21～16．10）。结论CYP1A16235C等位基因、GSTM1和T1缺陷基因型可影响机体对CRC的遗传易感性，前者是CRC的保护因素，后两者可使机体罹患CRC的风险增高。     

焦炉作业工人外周血淋巴细胞染色体损伤的遗传易感性研究

目的研究外源性化学物代谢酶基因多态性与焦炉作业工人外周血淋巴细胞染色体损伤的关系。方法选取149名焦炉作业工人和24名非职业多环芳烃(PAH)暴露人员作为研究对象,测定其尿中1-羟基芘浓度来反映PAH暴露的内剂量;对照组的外周血淋巴细胞微核水平的上4分位数(6‰)作为判断个体染色体损伤阳性的界值;分析CYP1A1、GSTM1、GSTT1、GSTP1、CYP2E1、NQO1、NAT2和mEH基因的多态性;使用多元logistic回归方程校正职业暴露情况、年龄、性别、吸烟和饮酒状况因素,计算不同基因型工人发生染色体损伤阳性的OR值,并探讨基因间的交互作用。结果调整了173名研究对象的职业暴露、年龄、性别、吸烟和饮酒状况后,GSTM1缺失基因型个体染色体损伤危险度显著性增加(调整OR=2．01,95％CI=1．03—3.91);与NQO1基因P187S位点野生型纯合子个体比较,变异型纯合子个体染色体损伤危险度显著性增加(调整OR=3．18,95％CI=1．18—8．62);与mEH基因H113Y位点野生型纯合子个体比较,变异型纯合子个体染色体损伤危险度显著性降低(调整OR=0．40,95％CI=0.19～0．88);未发现其他基因的遗传变异与研究对象外周血淋巴细胞染色体损伤危险度的显著关联。此外,还发现GSTM1、NQO1基因P187S位点和mEH基因H113Y位点的遗传变异对染色体损伤危险度的影响中存在基因-基因交互作用。结论本研究发现GSTM1、NQO1和mEH基因的遗传变异可显著性影响职业PAH暴露个体外周血淋巴细胞染色体损伤危险度,并存在基因一基因交互作用。     

微粒体环氧化物水化酶基因多态性对焦炉工尿中1-羟基芘水平的影响

目的　研究外源性化学物代谢酶基因多态性与焦炉工尿中 1 羟基芘水平的关系。方法　分别选取 14 8名焦炉工和 6 9名非职业多环芳烃 (PAHs)暴露人员作为研究对象 ,使用碱水解 -高效液相色谱法测定其尿中 1 羟基芘浓度 ;分析了CYP1A1基因第 7外显子I4 6 2V位点、GSTM1、GSTT1、GSTP1基因I10 5V位点、CYP2E1基因 5’非编码区的Pst1位点和第 6内含子的Dra1位点、NQO1基因P187S位点、NAT2基因Kpn1、BamH1和Taq1位点以及mEH基因H113Y和R139H位点的多态性 ;使用调查表收集个人职业暴露史、年龄、性别、吸烟和饮酒等信息。结果　焦炉工尿中 1 羟基芘水平[(5 .6 1± 1.0 4 ) μmol molCr]高于对照组 [(0 .74± 0 .32 ) μmol molCr],差异有显著性 (P <0 .0 5 )。调整了PAHs外暴露等级和吸烟因素后 ,焦炉工中具有mEH基因 113位点变异纯合子基因型个体尿中1 羟基芘水平高于杂合子和野生型纯合子 (6 .4 1± 1.0 9>6 .2 4± 1.0 9>4 .6 2± 0 .95 μmol molCr) ,且野生型纯合子与变异型纯合子基因型个体间尿中 1 羟基芘水平的差异有显著性 (P <0 .0 5 )。在焦炉工中还发现CYP1A1和mEH基因多态性存在交互作用。结论　mEH基因 113位点的基因多态性可明显影响焦炉工尿中 1 羟基芘水平。     

Bladder cancer, GSTs, NAT1, NAT2, SULT1A1, XRCC1, XRCC3, XPD genetic polymorphisms and coffee consumption: a case–control study

The aim of the study was to investigate NAT1, NAT2, GSTM1, GSTT1, GSTP1, SULT1A1, XRCC1, XRCC3 and XPD genetic polymorphisms, coffee consumption and risk of bladder cancer (BC) through a hospital-based case–control study. The study population included 197 incident BC cases and 211 controls. The association between genetic polymorphisms, coffee drinking and BC risk was assessed by logistic regression taking into account age, education, tobacco smoking and occupational exposures to polycyclic aromatic hydrocarbons and aromatic amines. No association was found between the genetic polymorphisms investigated and BC risk according to coffee consumption apart of a significant increased BC risk among GSTP1 105-114 Val carriers heavy coffee drinkers (>3 cups/day) (OR 3.18, 95%CI 1.06–9.55). In conclusion our findings suggest a very limited role, if any, of genetic polymorphisms investigated in modulating the BC risk in coffee drinkers.     

Aromatic DNA adducts in coke-oven workers, in relation to exposure, lifestyle and genetic polymorphism of metabolic enzymes

Objective: This study investigates the effect of multiple factors, including exposure to polycyclic aromatic hydrocarbons (PAHs), lifestyle, genetic polymorphism of cytochrome P450 (CYP)1A1, glutathione transferase (GST)M1, GSTP1, N-acetyltransferase (NAT)2 and gene p53, as well as any family history of cancer, on DNA adduct levels in coke-oven workers. Methods: Sixty-five coke-oven workers employed at the largest iron-steel factory in China were recruited for the study. Personal data were collected at the interview. DNA adduct levels in total white blood cells (WBCs) were detected using ³²P-postlabeling techniques. Genetic polymorphisms were analyzed by polymerase chain reaction (PCR) methods. Results: The subjects were divided into low and high exposure groups, according to personal exposure to PAHs. The mean adduct value was 1.57 (range 0.54 to 4.35) per 10⁸ nucleotides. A tendency for increased levels of DNA adducts in the high exposure group was observed, compared with the low exposure group (P = 0.07). In the low exposure group, DNA adducts were found to be positively associated with urinary cotinine (r = 0.44, P = 0.01). The rare allele homozygotes of CYP1A1 showed significantly higher DNA adduct levels than those of other CYP1A1 genotypes. Individuals with the NAT2 wild type had significantly increased DNA adduct levels than those with other NAT2 genotypes in the high exposure group. The p53 genetic polymorphism revealed a significantly positive effect on DNA adducts formation. There was a significantly higher adduct level in the subjects with a family history of cancer than those without, in the high exposure category. Conclusions: Effects of several variables, such as smoking, genetic polymorphism of 2 CYP1A1, NAT2, and gene p53, and a family history of cancer on DNA adduct levels were found, suggesting that these variables should be considered when evaluating the genotoxic effect of occupational exposure to PAHs using WBCs DNA adducts. Received: 15 February 1999 / Accepted: 15 June 1999     

Genetic polymorphisms and chromosome damage.

Genetic polymorphisms that affect xenobiotic metabolism or cellular response to DNA damage can modulate individual sensitivity to genotoxins. Information on the effects of such polymorphisms on the level of chromosome damage may facilitate the identification of risk groups and increase the sensitivity of cytogenetic endpoints as biomarkers of genotoxic exposure and effect. Glutathione S-transferase M1 (GSTM1) is an important detoxification enzyme which, due to a homozygous gene deletion (null genotype), is lacking from about 50% of Caucasians. A higher level of DNA adducts and chromosome damage has been detected in lymphocytes of tobacco smokers and bus drivers who lack the GSTM1 gene. Other polymorphic glutathione S-transferases include GSTM3, GSTP1, and GSTT1. The GSTT1 null genotype (10-20% of Caucasians) has been associated with an increased "baseline" level of sister chromatid exchanges (SCEs) in lymphocytes. N-acetyltransferase 2 (NAT2), metabolizing xenobiotics with primary aromatic amine and hydrazine structures, is another important polymorphic phase II enzyme. Subjects having the NAT2 slow acetylator genotype appear to show an increased baseline frequency of lymphocyte CAs in the absence of identified environmental exposure. Besides human biomonitoring studies, genetic polymorphisms may be important in explaining individual variation in genotoxic response observed in genetic toxicology tests with human cells. Several studies have suggested that blood cultures from GSTT1 null and GSTM1 null individuals have increased in vitro sensitivity to various genotoxins. The best-known example is probably the diepoxybutane sensitivity of GSTT1 null donors. Recently discovered polymorphisms affecting DNA repair may be expected to be of special importance in modulating genotoxic effects; the first available studies have suggested that the exon 10 Arg399Gln polymorphism of XRCC1 gene (X-ray repair cross-complementing group 1) could affect individual genotoxic response. In conclusion, the genetic polymorphism of GSTM1 influences the frequency of chromosome damage in exposed humans, while that of GSTT1 and NAT2 affect the "baseline" level of such damage. Both GSTM1 and GSTT1 genotypes may shape the in vitro genotoxic response of human lymphocytes. The significance of DNA repair polymorphisms is presently unclear.     

氯乙烯作业工人染色体损伤及其遗传易感性

目的 探讨氯乙烯(VCM)致染色体损伤与DNA修复基因和代谢酶基因多态间的关系.方法 收集上海某化工厂402名VCM接触工人健康体检资料、人口学资料(年龄和性别)、生活方式(吸烟、饮酒)和职业接触等因素,评估个人VCM累积接触剂量并分组.采集静脉血3 ml,采用外周血淋巴细胞胞质分裂阻滞微核试验(CBMN)检测染色体损伤,采用聚合酶链式反应(PCR)检测GSTT1、GSTM1基因缺失情况,采用PCR-限制性片段长度多态性技术(RFLP)检测其他基因多态.结果 多元Poisson回归分析结果表明,中(4000～40000 mg)、高(＞40000 mg)VCM接触剂量组染色体损伤的风险明显高于低剂量组,调整后的FR值分别为1.19(1.06～1.34)和1.20(1.06～1.38),差异有统计学意义(P值分别为0.003和0.01);携带CYP2E1和XRCC1 Arg280His突变型基因的个体微核率明显高于野生型个体,调整后的FR值分别为1.12(1.02～1.23)和1.13(1.02～1.25),差异有统计学意义(P值均为0.02);携带GSTP1Val/Val和ALDH2 Glu/Glu基因型个体微核率明显高于其他基因型个体,调整后的FR值分别为0.74(0.59～0.94)和0.87(0.79～0.95),差异有统计学意义(P值分别为0.01和0.003).结论 VCM致染色体损伤与VCM累积接触剂量增高及GSTP1 Val/Val、CYP21E1 c1c2/c2c2、ALDH2 Glu/Glu、XRCC1 280His/His 或Arg/His基因型多态性等因素有关.开展VCM致染色体损伤与遗传易感性方面的研究,有助于VCM致癌机制的阐明,而研究中易感性多态位点的发现也可以为识别易感人群提供理论依据.     

Re-assessment of the influence of polymorphisms of phase-II metabolic enzymes on renal cell cancer risk of trichloroethylene-exposed workers

Problem Individual differences in susceptibility to trichloroethylene-induced nephrocarcinogenicity may be conferred by genetic polymorphisms of glutathione S-transferases (GST), because enzymes of this group are pivotal for the metabolic activation of trichloroethylene. Because of a potential involvement of N-acetylation in the detoxication of reactive trichloroethylene metabolite(s) to N-acetyl-cysteine derivatives, polymorphisms of the NAT2 gene may also be relevant. Methods The primary collective used for a re-investigation of these questions was that of a hospital-based case-control study by Brüning et al. (Am J Ind Med 43:274–285, 2003) of 134 renal cell cancer cases (20 cases exposed to trichloroethylene) and 401 matched controls. Genetic polymorphisms of GSTT1, GSTM1, GSTP1 and NAT2 were studied. Additional control collectives of non-diseased persons were used for comparison of allele frequencies. Results No genetic influences on the development of renal cancer due to trichloroethylene were apparent, related to the deletion polymorphisms of GSTT1 and GSTM1, as well as to the NAT2 rapid/slow acetylator states. However, renal cell cancer cases displayed a somewhat higher proportion of the homozygous GSTP1 313A wild type (GSTP1*A), although this was not statistically significant (χ² test: P = 0.1071, when using only the original controls of Brüning et al. (2003); P = 0.0781 with inclusion of the additional controls). Conclusion The re-investigation does not confirm the working hypothesis of an influence of the deletion polymorphisms of the glutathione S-transferases GSTT1 and GSTM1 on renal cell cancer development due to high occupational exposures to trichloroethylene.     

Impairment of colour vision in workers exposed to organic solvents

OBJECTIVES—To investigate loss of colour vision related to exposure to solvents and the role of three enzyme polymorphisms in modifying the risk in exposed workers.
METHODS—A sample was studied of 68 male dockyard workers and 42 male community controls with and without neuropsychological symptoms from a previous cross sectional study. Indices of cumulative and intensity based exposure to solvents were calculated for all subjects. Alcohol, drug, and smoking histories were obtained. Colour vision was tested by Lanthony D15d colour vision test. Genotype of glutathione S-transferase M1 and T1 and N-acetyltransferase 2 polymorphisms were determined.
RESULTS—The relation between impairment of colour vision and exposure to solvents was investigated with multiple regression techniques. Increasing annual exposure to solvents was significantly associated with reduced colour vision (p=0.029). Impairment of colour vision was not associated with neuropsychological symptoms as measured by the Q16 solvent symptom questionnaire. No significant association was found between acquired impairment of colour vision and genetic polymorphisms when GSTM1, GSTT1 or NAT2 phenotypes were included in the analyses.
CONCLUSIONS—Exposure to mixed solvents is associated with impairment in colour vision, the risk increases with increasing exposure. The risk of impairment of colour vision was not altered in this study by the presence of different GSTM1, GSTT1 or NAT2 polymorphisms.


Keywords: colour vision; organic solvents; genetic polymorphisms     

DDB2基因单核苷酸多态性与焦炉工外周血淋巴细胞DNA损伤的关联

[目的]探讨DDB2基因单核苷酸多态性与焦炉工外周血淋巴细胞DNA损伤的关联。[方法]选取焦化厂在岗焦炉工325名作为接触组,选择同厂无职业多环芳烃暴露者150人作为对照组,使用反向高效液相色谱法测定尿1-羟基芘含量,采用碱性单细胞凝胶电泳技术检测淋巴细胞DNA损伤情况,应用TaqMan探针荧光标记聚合酶链反应方法对DDB2基因进行分型。[结果]接触组尿1-羟基芘含量[（4.41±1.06）μmol/mol肌酐]高于对照组[（3.33±1.03）μmol/mol肌酐],差异有统计学意义（P〈0.05）;接触组外周血淋巴细胞彗星尾距（olive tail moment,OTM）[0.41（0.08～4.28）]也高于对照组[0.31（0.08～3.16）],差异有统计学意义（P〈0.05）。两组中DDB2基因SNPs的不同基因型携带者OTM差异均无统计学意义。分层结果表明,对照组年龄〈39岁个体中,启动子区rs2029298位点AA基因型携带者DNA损伤高于GG基因型携带者,差异有统计学意义（P〈0.05）;其他差异均无统计学意义。[结论]DDB2基因多态性对焦炉工外周血淋巴细胞DNA损伤程度无影响,在对照组低年龄个体中rs2029298位点AA基因型携带者的DNA损伤程度高于GG基因型携带者。