甲醛对暴露工人外周血淋巴细胞的遗传损伤作用

目的评价甲醛对暴露工人外周血淋巴细胞染色体和DNA损伤水平。方法选择65名甲醛暴露工人和非甲醛暴露工人70名为研究对象，采用甲基纤维素法和单细胞凝胶电泳法，分析其外周血淋巴细胞微核发生率和DNA断裂损伤。结果暴露组工人外周血淋巴细胞微核发生率、DNA断裂损伤的细胞数，与对照组比较，差异有统计学意义（P〈0．05），并有随工龄、暴露浓度增加而增高的趋势。但甲醛浓度为0．5mg／m^3～3．11mg／m^3时，DNA断裂损伤细胞与对照组比较，差异无统计学意义（P〉0．05）。结论甲醛暴露可导致工人外周血淋巴细胞染色体和DNA断裂损伤明显增高，DNA断裂可望成为暴露人群的早期效应标志物和致癌机制之一。     

八氯二丙醚暴露工人微核及DNA损伤程度

的了解八氯二丙醚暴露可能对工人造成的健康危害。方法对八氯二丙醚（S2）生产工人进行流行病学调查，并采集外周血进行微核（MN）和单细胞凝胶电泳试验（SCGE），了解S2可能对工人健康的损伤。结果八氯二丙醚接触者外周血微核发生率较对照组无明显增加（P〉0．05），DNA表现出不同程度的损伤（P〈0．01）。结论目前S2生产车间有害气体的暴露水平对工人外周血DNA有一定的损伤作用。     

焦化作业工人淋巴细胞HSP70表达及作用

目的探讨热应激蛋白70（HSP70）在焦炉工人外周血淋巴细胞的表达水平及其意义。方法用微核试验和碱性单细胞凝胶电泳技术（彗星试验）检测淋巴细胞的染色体畸变和DNA损伤情况，用蛋白印迹（westem blot）法检测淋巴细胞HSP70表达水平。结果外周血淋巴细胞微核率和彗星尾长在高暴露组显著高于对照组，差异有统计学意义（P〈0．05）；HSP70的表达水平在高暴露组、低暴露组和对照组分别为1．12±0．36。1．34±0．83。0．89±0．40，低暴露组明显高于对照组（P〈0．05）；高暴露组工人的外周血淋巴细胞HSP70的表达水平与彗星尾长呈负相关（r=-0．416，P=0．03）。结论焦炉作业环境可诱发外周血淋巴细胞HSP70蛋白表达，较高水平HSP70的表达对细胞DNA损伤具有保护作用。     

焦炉工人外周血淋巴细胞热休克蛋白72水平及与DNA损伤的关系

目的研究焦炉逸散物对焦炉工人外周血淋巴细胞热休克蛋白72（Hsp72）水平的影响及与DNA损伤的关系，探讨Hsp72在细胞损伤保护中的意义。方法选取267名焦炉工人和30名对照，以Western blot法检测外周血淋巴细胞Hsp72的水平，彗星试验检测DNA损伤水平，个体采样采集作业环境空气样本，高效液相色谱法测定环境苯并[a]芘浓度。结果高暴露组工人外周血淋巴细胞Hsp72水平（G±SG）和Olive尾矩（G±SG）分别为1．24±0．42和4．49±1．24，明显高于低暴露组（1．01±0．35和2．99±1．10）和对照组（0．85±0．34和2．40±1．00），差异有统计学意义（P〈0．05）。以全体研究对象Hsp72中位数为界值，将研究对象分为Hsp72高表达组和低表达组，Hsp72高表达的人数相对比率在对照组、低暴露组、高暴露组分别为36．7％、43．1％和58．3％，呈逐渐增高趋势，差异有统计学意义（P=0．003）。在Hsp72高表达组，Hsp72表达水平随着暴露等级升高而升高，其中高暴露组与对照组的差异有统计学意义（P〈0．05），但各组之间Olive尾矩的差异无统计学意义（P〉0．05）。在Hsp72低表达组中，各组Hsp72水平的差异无统计学意义（P〉0．05），而Olive尾矩随暴露等级升高而升高，其中高暴露组与低暴露组和对照组比较，差异有统计学意义（P〈0．01），且明显高于Hsp72高表达组的高暴露组工人。高暴露组Hsp72水平与Olive尾矩呈负相关（r=0．503，P〈0．01）。结论焦炉逸散物可诱导焦炉工人外周血淋巴细胞Hsp72水平升高，Hsp72对细胞DNA损伤具有保护作用。     

焦炉逸散物对作业工人细胞遗传毒性损伤的研究

为探讨焦炉逸散物对作业工人细胞遗传物质的毒性损伤，寻找职业性肺癌的早期监测指标，选择炉顶作业工人167人，炉侧作业工人123人，辅助作业工人27人。每种作业按暴露工龄分为三组。不接触有害物质的作业工人336人为对照组。用微核检测法和单细胞凝胶电泳技术分别对外周血淋巴细胞微核和DNA损伤进行测定。结果显示，炉顶、炉侧作业区组的微核率均高于辅助作业区组和对照组，差异有极显著性（P＜0．01）；炉顶、炉侧11～20年组的＋级损伤与＞20年组的＋＋级损伤均高于对照组，差异有极显著性（P＜0．01），且随着工龄的的延长DNA损伤加重。结果表明，长期接触焦炉逸散物可损伤作业工人的遗传物质DNA，影响工人的健康。提示微核检测法和单细胞凝胶电泳技术相结合作为早期监测指标更好。     

长春新碱诱发的人淋巴细胞遗传损伤的体外试验方法评价

目的 用3个遗传终点来评价人外周血淋巴细胞暴露于不同剂量长春新碱（VCR）后的遗传损伤。方法 外周血来自男女2名助血员，用终浓度为0．00（溶剂对照）、0．01、0．02、0．04、0．08μg／ml的VCR染毒24h，再用微核试验、彗星试验和hprt基因突变试验检测淋巴细胞的遗传损伤。微核试验以微核率、微核细胞率、核芽、核质桥、核分裂指数和凋亡细胞作为染色体损伤指标；彗星试验以平均尾长和平均尾相作为DNA损伤的指标；hprt基因突变试验以基因突变率作为评价指标。结果 3种试验均呈阳性。hprt基因突变率和凋亡细胞数从0．02μg／ml剂量开始与对照的差异有统计学意义（P〈0．05或P〈0．01），其余指标从最低剂量组开始就明显高于对照组，差异均有统计学意义（P〈0．01或P〈0．05），并存在剂量一效应关系。结论 VCR在体外可通过不同机制诱发人淋巴细胞的遗传损伤。     

低浓度苯系物暴露与加油站工人淋巴细胞遗传损伤的关系研究

目的探讨低剂量接触苯系物对加油站工人外周血淋巴细胞的DNA损伤作用。方法采用彗星试验检测加油站暴露组与对照组工人外周静脉血淋巴细胞DNA损伤,采用气相色谱-质谱法检测相应工作区空气中苯系物的浓度。结果暴露区苯、甲苯、乙苯、二甲苯浓度均高于对照区(P0.001);暴露组彗星尾矩和Olive尾矩均高于对照组,差异均有统计学意义(P0.05)。结论长期低浓度苯系物暴露可能导致加油站工人淋巴细胞DNA遗传损伤。     

微核试验和彗星试验观察职业性二甲基乙酰胺暴露的遗传损伤

[目的]观察二甲基乙酰胺（DMAc）对职业接触人群所产生的遗传损伤。[方法]用胞质阻断微核试验（CBMN）和彗星试验（SCGE）检测某氨纶企业DMAc接触工人（30名）及非接触DMAc的对照人员（30名）的外周血淋巴细胞DNA和染色体损伤。[结果]接触组微核率、微核细胞率、核分裂指数分别为（4．67±2．25）％。、（4．56±2．19）‰、（1．82±0．30）％。,对照组分别为（5．00±2．62）％。、（4．89±2．59）‰、（1．73士0．25）％。,两组的各指标间差异均无统计学意义（P〉0．05）。接触组彗星尾DNA百分比、细胞尾长、尾相分别为（4．76±2．63）％、（12．60±5．68）岍、（2．51±2．30）,对照组分别为（4．49±2．48）％、（11．77±5．01）um、（2．28±1．89）,各指标间的差异均无统计学意义（P〉0．05）。[结论]在本实验条件下,职业性DMAc接触人群外周血淋巴细胞的染色体和DNA未表现出遗传损伤。     

焦化厂工人ERCC8基因多态性与外周血淋巴细胞DNA损伤的关系

[目的]探讨焦化厂工人ERCC8基因多态性与外周血淋巴细胞DNA损伤的关系。[方法]选择某焦化厂多环芳烃（PAHs）接触者207名焦炉作业工人和115名无PAHs接触及其他毒物暴露者，采集外周静脉血，分离淋巴细胞，使用单细胞凝胶电泳实验观察DNA损伤情况；采用TaqMan—MGB探针检测ERCC8基因分型；运用PHASE2．0．2遗传分析软件计算单倍型。[结果]接触组外周血淋巴细胞的Olive尾矩（Olive Tail Moment，OTM）高于对照组（经对数转换后分别为1．25±1．17和0．53±0．98），差异有极显著性（P〈0．01）。在接触组中，ERCC8基因Rs3117位点CT＋CC和TT基因型携带者外周血淋巴细胞的OTM分别为1．57±1．13和1．15±1．67，差异有统计学意义（P〈0．05）；启动区Rs158920位点CT＋TT和CC基因型携带者外周血淋巴细胞的OTM分别为1．14±1．21和1．24±1，17，差异无统计学意义（P〉0．05）。对照组中相应位点的OTM分别为0．54±0．93和0．56±1．00以及0．52±0．86和0．54±1．02，差异均无统计学意义（P〉0．05）。在接触组中，两个位点组成的单倍型对中CT／CT单倍型对和其他单倍型对携带者外周血淋巴细胞的OTM分别为1．20±1．17和1．36±1．17；对照组分别为0．54±1．02和0．51±0．91，两组差异均无统计学意义。[结论]接触组外周血淋巴细胞ERCC8基因Rs3117位点的不同基因型和DNA损伤的严重程度有关联。     

甲基叔丁基醚职业暴露人群淋巴细胞遗传损伤研究

目的研究甲基叔丁基醚(MTBE)暴露对淋巴细胞遗传毒性损伤,为建立MTBE职业人群暴露限值体系提供参考。方法人B淋巴母细胞分别用不同浓度MTBE溶液染毒24 h,彗星实验检测细胞尾部DNA百分比及Olive尾矩,Annexin V-FITC/PI双染流式细胞术检测细胞凋亡百分比。选择某炼化厂60名MTBE职业暴露工人为暴露组,55名未接触MTBE工人为对照组,微核实验检测外周血淋巴细胞微核率,彗星实验检测外周血淋巴细胞尾部DNA百分比及Olive尾矩,酶联免疫吸附试验检测外周血血浆丙二醛(MDA)、8-羟基脱氧鸟苷(8-OHd G)及谷胱甘肽-过氧化物酶(GSH-Px)水平。结果人B淋巴母细胞经10、12.5μmol/L的MTBE染毒24 h后,尾部DNA百分比、Olive尾矩和细胞凋亡百分比均高于对照组(P0.05)。暴露组工人外周血微核阳性率为8.93%,高于对照组的3.92%,但差异无统计学意义(P0.05);暴露组尾部DNA百分比为(15.70±7.67)%,高于对照组的(14.65±6.20)%,差异无统计学意义(P0.05);暴露组Olive尾矩为7.00±4.94,高于对照组的3.84±1.97(P0.01);暴露组与对照组工人血浆MDA、8-OHd G及GSH-Px水平差异均无统计学意义(P0.05)。结论MTBE暴露可诱导人B淋巴母细胞和人外周血淋巴细胞发生遗传损伤。     

Primary DNA damage in peripheral mononuclear blood cells of workers exposed to bitumen-based products

The genotoxic effect of occupational exposure to bitumen-based products was determined by the extent of DNA strand breaks and alkali-labile sites of the DNA of peripheral mononuclear blood cells from seven roofers, 18 road paving workers, and nine bitumen painters. In order to evaluate short-term genotoxic effect the workers were investigated on Fridays and on Mondays after a weekend free of occupational exposure. The roofers (all cigarette smokers) showed a significantly (P < 0.002) 43% higher mean level of alkaline DNA strand breaks on Friday than did the ten smoking controls included in this study. Also, comparison of the individual levels of alkaline strand breaks on Mondays and on Fridays revealed a significant increase (P < 0.05, Wilcoxon test) during the work week. In the road paving workers and the bitumen painters no statistically significant difference in the mean levels of alkaline strand breaks could be found compared to controls either for the measurement on Mondays or for that on Fridays. However, interesting tendencies were observed. As in the group of roofers, the mean level of alkaline DNA strand breaks as well as the majority of the individual levels of alkaline strand breaks of road paving workers was higher on Fridays than on Mondays. In contrast, bitumen painters exhibited a relatively high level of alkaline DNA strand breaks on Mondays and a decreased mean level of strand breaks on Fridays. DNA adducts could be detected at a low level (up to 2.9 adducts per 10⁹ bases) in 10 of 14 road paving workers and bitumen painters using the ³²p-postlabelling assay. The number of DNA adducts correlated with the years spent in the present job. Road paving workers and bitumen painters showed only suggestive evidence for a possible genotoxic effect due to their occupational exposure. Because we cannot exclude the formation of DNA cross-links in these workers, a more detailed investigation of the hazard is urgently needed. For roofers, substantial genotoxic damage in peripheral mononuclear blood cells was observed in this study.This study contains parts of an M.D. thesis by G. Boettler     

甲醛危害的人群研究(待续)

该文概要讲述了甲醛在人体内的代谢,甲醛的职业暴露和其对职业人群健康的危害。着重阐述了甲醛的遗传毒性及国内外甲醛与癌的职业流行病学研究方法、思路及主要成果。对鼻咽癌虽偶有阴性结果,但2004年IARC已确认甲醛可致人鼻咽癌。其他呼吸系统癌,正反结果都有,说明尚需进一步研究;白血病及其他系统癌,仍需积累更多的职业人群资料。由于甲醛的职业接触人群广泛,且居住环境尤其室内环境普遍存在甲醛,其致癌性的研究将是今后长期而艰巨的任务。     

可溶性铬盐职业接触者DNA链断裂的研究

目的通过对职业接触可溶性铬盐人群外周血淋巴细胞DNA链断裂水平的研究,了解该生物指标在职业人群中分布的水平、特点及其影响因素,探讨其作为职业接触铬盐人群生物标志物的可行性,为职业接触铬盐劳动者生物监测及健康危险性评价提供理论依据。方法本研究利用横断面现场研究,对山东省济南市某铬盐生产企业进行了流行病学调查。接触组选择重铬酸钾制造业铬盐作业健康劳动者114名(男74名、女40名),对照组为无毒物接触史的健康农民30名(男22名、女8名),两组人群在年龄、性别和吸烟状况等方面相匹配。通过问卷调查了解研究对象的一般情况、职业暴露情况、饮酒吸烟情况、既往疾病史(用药史)、急性感染情况、个人防护情况等。利用单细胞凝胶电泳法,检测外周血淋巴细胞DNA链断裂水平,并通过计算加权分评价损伤程度;作业环境铬盐浓度的测定采用双滤膜个体采样器8 h工作日连续采样,滤膜铬盐含量采用火焰原子吸收分光光度法测定;红细胞中铬浓度测定采用石墨炉原子吸收分光光度法。用SPSS10.0统计软件进行多元回归分析。结果(1)职业接触可溶性铬盐劳动者外周血淋巴细胞DNA链断裂水平得分为54.52±23.51,高于对照组的24.70±11.84,有统计学意义(P<0.01)。(2)当空气中个体铬盐暴露浓度小于106.00μg/m3时,职业接触可溶性铬盐劳动者DNA链断裂水平,随个体铬盐暴露水平的增加而增加,并呈明显的剂量-反应关系。(3)相关分析结果表明:外周血淋巴细胞DNA链断裂水平与空气中个体铬盐暴露水平、红细胞中铬浓度水平均呈显著的正相关性(P<0.01)。(4)多元回归证实:在α=0.10水平上,吸烟剂量、空气中铬盐浓度、接触铬盐的年限对淋巴细胞DNA链断裂水平影响显著。结论DNA链断裂可以作为职业接触可溶性铬盐劳动者遗传损伤效应性生物标志物,可望用于职业接触可溶性铬盐劳动者生物监测及健康危险性的评价。     

Biological monitoring the exposure to polycyclic aromatic hydrocarbons of coke oven workers in relation to smoking and genetic polymorphisms for GSTM1 and GSTT1.

Occupational exposure to polycyclic aromatic hydrocarbons (PAH) increases the risk of developing lung cancer. Human exposure is often demonstrated by increased internal levels of PAH metabolites and of markers for early biological effects, like DNA adducts and cytogenetic aberrations.Objective: This study aimed to assess whether the current exposure to PAH of coke oven workers in a Dutch plant induced biological effects, and to determine if these effects are influenced by tobacco smoking and by genetic polymorphisms for the glutathione S-transferase genes GSTM1 and GSTT1.Methods: Urinary 1-hydroxypyrene (1-OHpyr) levels were used to monitor the internal dose, while the internal effective dose was assessed by monitoring PAH-DNA adducts, DNA strand breaks (Comet assay), sister-chromatid exchanges (SCE) and cells with a high frequency of SCE (HFC) in lymphocytes together with micronuclei (MN) in exfoliated urothelial cells.Results: Occupational exposure to PAH resulted in statistically significant increased 1-OHpyr levels (P<0.001), but it did not cause a significant induction of SCE, HFC, MN, DNA strand breaks or DNA adducts. Smoking caused a significant increase of 1-OHpyr (P<0.05), SCE (P<0.001), HFC (P<0.001) and DNA adducts (P<0.05), but not of MN or DNA strand breaks. Following correction for the smoking-related effects, no occupational induction of the effect biomarkers could be discerned. Multi-variate analysis did not show a significant influence of GSTM1 and GSTT1 polymorphisms on any biomarker. Also no significant interactions were observed between the various biomarkers.Conclusion: This study shows that in the examined plant, the occupational exposure to PAH does not result in measurable early biological effects     

Biomonitoring of DNA damage by alkaline filter elution

Summary The majority of DNA lesions resulting from interactions of carcinogens with DNA are usually either single strand breaks or lesions which are converted to single strand breaks by treatment of DNA with alkaline solutions. A sensitive method of detecting DNA single strand breaks is the alkaline filter elution of DNA. We started to test this method for biomonitoring occupational exposure with sensitive experimental conditions using pH 12.6, where most alkali-labile DNA lesions are converted to single strand breaks. Under our conditions statistically significant differences can be detected between the elution rates of untreated V79 cells and cells treated with [³H]-thymidine 24 h prior to the elution. Statistically significant increases were detected in the elution rates of male smoking automobile mechanics and male smoking painters compared to non-smoking controls. No statistically significant differences were detected in the elution rates of male non-smoking automobile mechanics and male workers with a suspected exposure to halogenated aromatics compared to male controls. No statistically significant differences were observed in the elution rates of female smoking dry-cleaning workers compared to female smoking controls. Our experience showed that the alkaline elution technique can be a valuable tool for monitoring DNA damage in peripheral lymphocytes in man.Supported by the Bundesministerium fur Forschung und Technologie grant 01HK354 0This study contains part of an M.D. Thesis     

Magnetic-field-induced DNA strand breaks in brain cells of the rat

In previous research, we found that rats acutely (2 hr) exposed to a 60-Hz sinusoidal magnetic field at intensities of 0.1-0.5 millitesla (mT) showed increases in DNA single- and double-strand breaks in their brain cells. Further research showed that these effects could be blocked by pretreating the rats with the free radical scavengers melatonin and N-tert-butyl-alpha-phenylnitrone, suggesting the involvement of free radicals. In the present study, effects of magnetic field exposure on brain cell DNA in the rat were further investigated. Exposure to a 60-Hz magnetic field at 0.01 mT for 24 hr caused a significant increase in DNA single- and double-strand breaks. Prolonging the exposure to 48 hr caused a larger increase. This indicates that the effect is cumulative. In addition, treatment with Trolox (a vitamin E analog) or 7-nitroindazole (a nitric oxide synthase inhibitor) blocked magnetic-field-induced DNA strand breaks. These data further support a role of free radicals on the effects of magnetic fields. Treatment with the iron chelator deferiprone also blocked the effects of magnetic fields on brain cell DNA, suggesting the involvement of iron. Acute magnetic field exposure increased apoptosis and necrosis of brain cells in the rat. We hypothesize that exposure to a 60-Hz magnetic field initiates an iron-mediated process (e.g., the Fenton reaction) that increases free radical formation in brain cells, leading to DNA strand breaks and cell death. This hypothesis could have an important implication for the possible health effects associated with exposure to extremely low-frequency magnetic fields in the public and occupational environments.     

DNA–Protein Crosslinks and Sister Chromatid Exchanges as Biomarkers of Exposure to Formaldehyde

Abstract

Formaldehyde is classified as a probable human carcinogen. DNA–protein crosslinks (DPCs) and sister chromatid exchanges. (SCEs) may represent early lesions in the carcinogenic process. The authors examined the OPCs and, SCEs in peripheral-blood lymphocytes of 12 and 13 workers exposed to formaldehyde and eight and 20 unexposed workers, respectively. The amounts of DPCs and SCEs in the exposed and the unexposed differed significantly after adjustment for smoking. There was a linear relationship between years of exposure and the amounts DPC and SCE. The authors conclude that the data indicate a possible Mechanism of carcinogenicity of formaldehyde, and that formaldehyde is mutagenic to humans. These results support the use of DPCs as a biomarker of occupational exposure to formaidehyde and to detect high risk populations for secondary prevention.     

Study of the genotoxic effects of exposure to cosmic radiation in flight personnel using cytogenetic and molecular techniques

BACKGROUND: The ever-increasing use of air travel suggests the need to study health risks in flight personnel, by means of correct exposure assessment and evaluation of genotoxic effects. OBJECTIVES: After taking into consideration occupational risk and possible confounding factors, we studied 48 pilots and flight technicians engaged on long-haul flights together with a control group of 48 ground staff, with the aim of evaluating genotoxic effects of cosmic radiation exposure. On 36/48 subjects we also evaluated the presence of DNA damage (single and double strand breaks). METHODS: Traditional cytogenetics, the micronucleus test and FISH analysis, were used to study chromosome aberrations, micronuclei and translocations. The Comet test was used to analyze direct DNA damage (single and double strand breaks). RESULTS: Our findings indicated a significant increase in gaps and breaks and a significant increase of frequency ratio for translocations in pilots compared to controls, but revealed a non-significant difference in unstable aberrations and micronuclei. The Comet test did not show any significant increase of DNA damage in flight personnel with respect to ground staff. CONCLUSIONS: The possibility of a correlation between translocations and cancer risk emphasizes the need to adopt preventive measures for air flight personnel.     

Use of molecular epidemiological techniques in a pilot study on workers exposed to chromium.

OBJECTIVES--Molecular epidemiological techniques, capable of detecting damage to DNA, were used to see if such damage occurred in the lymphocytes of a group of workers exposed to chromium. The two aims of this pilot study were to see if these new techniques might make useful biological monitoring tools for workers exposed to chromium and also, to help assess whether the current occupational exposure limit for chromium (VI) was sufficiently protective in this specific working situation. METHODS--Volunteer groups of 10 workers exposed to chromium and 10 non-exposed workers provided urine and blood samples towards the end of the working week. Chromium concentrations were measured in whole blood, plasma, lymphocytes, and urine. Lymphocytes were used to examine two forms of DNA damage in the two groups; these were the level of DNA strand breakage and, the production of 8-hydroxydeoxyguanosine. RESULTS--Chromium concentration in whole blood, plasma, and urine of workers exposed to chromium was significantly raised (P < 0.01) compared with non-exposed controls, but in isolated lymphocytes, there was only a modest but significant (P < 0.05) increase in chromium in the group exposed to chromium. There was no difference in the levels of DNA strand breaks or 8-hydroxydeoxyguanosine between the groups. Air monitoring for chromium was not undertaken but current levels for the group exposed to chromium were reported to be around 0.01 mg/m3, which is 20% of the current United Kingdom occupational exposure limit. CONCLUSIONS--We were unable to detect any damage in lymphocytic DNA due to exposure to chromium. This may have been due to the low chromium exposure (< 20% of the United Kingdom occupational exposure limit), the ability of plasma to detoxify chromium (VI) to chromium (III) before it reached the lymphocytes, or perhaps the insensitivity of the molecular techniques used. It is now important to test these and other such techniques on groups exposed to levels closer to the United Kingdom occupational exposure limit.     

DNA damage and repair in cells of lead exposed people

BACKGROUND: One of the main sources of occupational exposure to lead in Colombia is in workers of battery industries and lead smelters. Genotoxic studies in human populations exposed to this metal have had conflicting results; this type of study has not been reported in Colombia. METHODS: Genotoxic effects of lead were studied in blood cell samples from workers of electric battery factories exposed to lead compounds. Single strand breaks and interference with DNA repair processes after an in vitro exposure of x-rays (300 cGy) were analyzed using the Comet Assay. The battery workers (n = 43) and 13 people not occupationally exposed to lead compounds who were selected as a control group, were classified into four categories according to their blood lead level. RESULTS: A significant difference was observed in DNA damage before the x-rays exposure (basal) between the lowest and highest categories of lead (mean DNA migration 55.6 micro and 85.9 micro, respectively). Additionally, a significant difference in DNA migration was also found immediately after irradiation between the lowest and highest lead categories (mean DNA migration: 199.8 micro and 317.8 micro respectively). The DNA migrations at different times after irradiation did not show a significant difference among the different lead levels. CONCLUSIONS: We concluded that although the single strand breaks following irradiation were not affected by blood lead concentration, the metal seems to sensitize the cells to damage induced by other genotoxicants.