精索静脉曲张不育患者8-羟基脱氧鸟苷水平的检测分析

目的:检测人血清及精浆中8-羟基脱氧鸟苷(8-OHdG)水平,探讨男性精索静脉曲张(VC)患者体内氧化损伤情况。方法:对41例VC不育患者、33例正常生育者进行精液分析,用8-OHdG酶联免疫试剂盒检测两组对象血清及精浆中8-OHdG水平,采用Wilcoxon两样本比较法对数据进行统计分析。结果:正常生育组的精子浓度、前向活动率、存活率均高于VC不育组(P<0.05),血清8-OHdG水平(中位数34.83ng/ml)低于VC组(中位数76.87ng/ml,P<0.05),精浆8-OHdG水平(中位数18.51ng/ml)低于VC组(中位数22.19ng/ml,P<0.05)。血清中8-OHdG水平高于精浆(P<0.05)。血清8-OHdG水平与精子存活率、前向活动率呈负相关(γ=-0.293,P<0.05;γ=-0.243,P<0.05);精浆8-OHdG水平与精子存活率、前向活动率呈负相关(γ=-0.327,P<0.05;γ=-0.275,P<0.05);血清及精浆中8-OHdG水平与精子浓度、正常形态率不相关。结论:VC患者血清和精浆中8-OHdG水平高于正常生育组,表明VC患者可能存在DNA氧化损伤,导致精子活力下降。     

燃煤型砷中毒患者症状分级和尿砷水平与尿中8-羟基脱氧鸟嘌呤核苷水平的相关性研究

目的研究燃煤型砷中毒患者症状分级和尿砷水平与尿中8-羟基脱氧鸟嘌呤核苷(8-OHdG)水平的相关性。方法对贵州省某燃煤型慢性地方性砷中毒病区进行调查,确定砷中毒患者并依据诊断标准进行症状分级(n=21)同时选择非砷暴露对照人群(n=6),测定尿中总砷(tAs)和8-OHdG水平。结果砷中毒患者组尿中tAs及8-OHdG水平均显著高于对照组,且重度患者组尿中tAs及8-OHdG水平均显著高于轻度和中度患者组。尿中8-OHdG水平与tAs水平呈显著正相关(r=0.590,P0.01);与砷中毒症状的轻重程度呈显著正相关(r=0.456,P0.05)。结论高砷暴露可引起尿8-OHdG水平增高,且呈剂量-效应关系;高砷暴露所致的损伤可能与氧化损伤关系密切。     

焦炉工人血清谷胱甘肽硫转移酶活力和尿8-羟基脱氧鸟苷水平

目的 探讨血清谷胱甘肽硫转移酶（GST）和尿8-羟基脱氧鸟苷（8-OHdG）作为焦炉工人多环芳烃（PAHs）暴露生物监测标志的可行性.方法 用高效液相色谱-电化学方法和试剂盒分别检测47名男性焦炉工和31名男性对照者尿8-OHdG水平和血清GST活力;尿1-羟基芘（1-OHP）作为PAHs接触的内暴露标志,采用碱水解-高效液相色谱方法分析.结果 焦炉工人尿1-OHP浓度的中位数（P25～P75）为[5.7（1.4～12.0）μmol/mol Cr],血清GST活力为[22.1（14.9～31.2）U/ml],尿8-O-HdG水平为[1.9（1.4～15.4）μmol/mol Cr],均高于对照组工人[3.0（0.5～6.4）μmol/mol Cr、13.1（9.5～16.7）U/ml、1.3（1.0～4.0）μmol/mol Cr],差异均有统计学意义（P＜0.05或P＜0.01）.以吸烟分层,两组工人尿1-OHP浓度和血清GST活力仅在吸烟者中、尿8-OHdG水平仅在非吸烟者中差异有统计学意义（均P＜0.01）.焦炉工人血清GST活力和尿1-OHP浓度呈正相关（rs=0.31,P＜0.01,n=78）.多元Logistic回归分析显示,与对照工人相比,焦炉工人血清GST活力＞16.7 U/ml和尿8-OHdG水平＞1.8 μmol/mol Cr的OR值分别为13.2和4.4;高体重指数是影响尿8-OHdG水平下降的独立因素.结论 焦炉工人血清GST活力增强和氧化性DNA损伤增加,吸烟和职业暴露有交互作用;血清GST有可能作为PAHs暴露评价的生物标志;尿8-OHdG检测有助于焦炉工肺癌危险度评价.     

北京市交警多环芳烃暴露及DNA氧化损伤水平研究

目的 了解北京市交警多环芳烃(PAHs)暴露对体内DNA氧化损伤水平的影响.方法 于2007年6-8月,以某城区41名男性外勤交警和34名男性郊区对照人群作为研究对象,进行问卷调查及环境空气PAHs浓度、内暴露指标尿中1-羟基芘(1-OHP)和DNA氧化损伤标志物尿中8-羟基脱氧鸟苷(8-OHdG)的检测,通过单因素及多元回归分析PAHs内外暴露水平对8-OHdG的影响.结果 交警组工作环境空气中细颗粒物(PM2.5)、苯并(a)芘[B(a)P]、PAHs浓度分别为0.096 mg/m3、3.20 ng/m3、38.32 ng/m3,高于郊区居民组相应值0.045 mg/m3、1.54 ng/m3、25.43ng/m3;交警组和郊区居民组人群尿中1-OHP浓度分别为(0.50±0.38)和(0.34±0.28)μmol/mol Cr(P＜0.05),尿中8-OHdG浓度分别为(13.74±6.30)和(11.61±6.02)ng/mg Cr(P＞0.05).多因素分析发现尿中1-OHP和吸烟是影响8-OHdG水平的重要因素,没有发现年龄、饮酒、锻炼习惯等调查因素对尿8-OHdG浓度的影响.结论 北京市交通污染对交警这一职业人群已产生一定的健康影响,环境空气PAHs暴露和吸烟是影响研究人群DNA氧化损伤水平的重要因素.     

太原市采暖期和非采暖期农村和城市居民尿中8-羟基脱氧鸟苷水平的比较研究

目的比较采暖期和非采暖期农村与城市居民体内DNA氧化损伤标志物8-羟基脱氧鸟苷(8-OHdG)的水平。方法分别于2009年10月(非采暖期)和2010年3月(采暖期),选择年龄在45～65周岁,在太原市居住时间≥5年的农村居民(傅山医院附近)79人和城市居民143人为研究对象,排除焦炉工等多环芳烃职业暴露者和癌症患者。采用ELISA试剂盒测定尿中8-OHdG的浓度。结果非采暖期农村居民尿中8-OHdG的浓度高于城市居民;采暖期农村居民尿中8-OHdG的浓度与城市居民无差别;在同一人群中,采暖期尿中8-OHdG的浓度高于非采暖期。结论太原市农村居民DNA氧化损伤水平高于城市居民,采暖期居民的DNA氧化损伤水平高于非采暖期。     

高效液相色谱-紫外法检测尿中8-羟基脱氧鸟苷

目的:观察利用高效液相色谱-紫外法检测尿液8-羟基脱氧鸟苷(8-OHdG)的效果.方法:尿液经前处理后,利用美国Agilent高效液相色谱仪检测8-OH-dG水平.结果:8-OHdG峰与杂质峰分离良好,8-OHdG浓度在0.5～20μg/ml之间旱良好线性,流动相最佳的pH为3.5,回收率在98.6%～100.1%之间,批内差异(CV)均低于8%.结论:高效液相色谱-紫外法是一种灵敏度较高、重复性好、易推广的尿液8-OHdG简便检测方法,值得推广.     

低浓度砷暴露者皮肤损害及DNA氧化损伤

目的 探讨女性慢性低浓度砷(As)暴露者皮肤损害情况及与DNA氧化损伤的关系.方法 选择山西大同某村长期饮水型低As暴露女性54人(病例组)和经济水平相近的邻村女性18人(对照组)作为研究对象,测定当地水As及研究对象体内尿As水平;并测定尿中8-羟基脱氧鸟苷(8-OHdG)水平.结果 低As暴露组人群体内尿As平均水平为(13.99±4.65) μg/gCr,尿8-OhdG平均水平为(8.61±4.51) ng/mgCr,均高于对照组(P＜0.05);尿中8-OHdG与尿As水平呈正相关(r=0.893,P＜0.05);尿中8-OHdG水平与水As暴露程度呈正相关(r=0.847,P＜0.05);尿8-OHdG水平较高者发生皮肤损害的危险性是较低者的2.838倍(OR =2.838,P＜0.05).结论 低浓度砷As暴露可致机体产生DNA氧化损伤;尿8-OHdG可作为一个稳定的As致氧化损伤生物标志物.     

介入放射工作人员血清8-羟基脱氧鸟苷水平分析

对50名介入放射工作人员（介入组）、50名非介入放射人员（普放组）和48名非放射人员（对照组）进行血清8-羟基脱氧鸟苷（8-OHdG）水平检测。结果显示，介入组血清8-OHdG水平高于普放组和对照组，差异具有统计学意义（均P<0.05），且随着年有效放射剂量及工龄的增加，血清8-OHdG水平呈上升趋势（均P<0.05）。提示长期低剂量电离辐射会引起介入放射工作人员血清8-OHdG水平升高，导致DNA氧化损伤。     

正常成人尿中8-羟基脱氧鸟苷水平的观察

目的检测正常成人尿中8-羟基脱氧鸟苷(8-OHdG)水平,了解其在正常人群中的分布范围.方法用8-OHdG的酶联免疫试剂盒检测尿中8-OHdG水平,用苦味酸法测定尿中的肌酐,计算8-OHdG的肌酐校正值.结果正常人群尿中8-OHdG水平为14.15±9.00ng/mgCr.在不同性别间存在显著性差异,男性为11.85±5.72ng/mgCr,女性为16.24±10.83ng/mgCr.按10岁一个年龄段分层,在男性、女性和全体人群中各年龄组间均无显著性差异.女性在21～60岁年龄段8-OHdG水平有随年龄增加而增高的趋势.结论正常人群8-OHdG水平的95%参考值范围在男女性分别为0～25.77ng/mgCr和0～44.89ng/mgCr.     

亚急性与慢性砷暴露人群尿砷和8-羟基脱氧鸟苷含量的比较

目的比较亚急性与慢性砷暴露人群尿砷水平、砷形态分布和DNA氧化损伤的情况。方法选择2004年12月阜新市亚急性砷中毒事件发生时阜新市中心医院收治的65名男性患者(年龄为20～62岁,水砷含量达48.5 mg/L,连续暴露4～7 d)为亚急性砷暴露组,慢性高砷(男性72人,年龄为18～73岁,水砷浓度为0.24 mg/L,暴露6 a)、低砷暴露人群(男性40人,年龄为18～60岁,水砷浓度为0.02 mg/L,暴露10 a,无砷中毒相关临床症状)均选自内蒙古呼和浩特市周边砷暴露区。采集亚急性砷暴露人群确诊入院且未采取治疗措施时的尿样,采集慢性砷暴露人群即时尿样。采用超低温捕集-氢化物发生-原子吸收分光光度法测定尿中不同形态砷含量,用酶联免疫法分析尿8-羟基脱氧鸟苷(8-OHdG)水平。结果3种不同砷暴露人群尿中总砷水平和不同形态砷水平均随着砷暴露剂量的升高呈升高趋势:亚急性砷暴露组>慢性高砷暴露组>慢性低砷暴露组,且差异均有统计学意义(P<0.05)。各组尿中无机砷、一甲基砷和二甲基砷含量占总砷含量的构成比(iAs%,MMA%和DMA%)间比较,差异均有统计学意义(P<0.05)。iAs%和MMA%在亚急性砷暴...     

8-Hydroxydeoxyguanosine in leukocyte DNA and urine of quartz-exposed workers and patients with silicosis

Objective: To examine radical-induced DNA damage and its elimination in workers exposed to quartz and in patients with silicosis, and to assess the relationship of these effects to lung function. Methods: Blood and spontaneous urine samples were obtained from active, quartz-exposed workers without silicosis (n=63), and from retired workers with silicosis (n=42). Levels of 8-hydroxydeoxyguanosine (8-OHdG) were determined in peripheral blood leukocyte DNA and urine, by the use of high-performance liquid chromatography coupled with ultra violet- (UV) and electrochemical detection. Results: No significant differences in the mean levels of 8-OHdG in leukocyte DNA and of urinary excretion of 8-OHdG were found between silicosis patients and quartz-exposed healthy workers. However, in the group of silicosis patients with increased oxidative DNA damage the urinary excretion of 8-OHdG was lower than in the corresponding group of active workers without silicosis. In the case of silicosis, urinary 8-OHdG correlated positively, and 8-OHdG in DNA correlated negatively, with forced expiratory volume in one second (FEV₁) and forced vital capacity (FVC). Healthy workers with a personally estimated high dust exposure in the workplace showed higher levels of 8-OHdG in DNA than did workers with moderate dust exposure. No association of 8-OHdG formation and/or elimination with duration of employment, field of activity, smoking or age was found. Conclusion: Our findings suggest that a less effective repair of 8-OHdG is associated with a higher degree of pulmonary airway obstruction in patients with silicosis. Received: 13 August 1999 / Accepted: 5 January 2000     

Urinary 8-hydroxy-2'-deoxyguanosine as a biomarker of oxidative DNA damage in workers exposed to fine particulates

Residual oil fly ash (ROFA) is a chemically complex mixture of compounds, including metals that are potentially carcinogenic because of their ability to cause oxidative injury. In this study, we investigated the association between exposure to particulate matter with an aerodynamic mass median diameter 相似文献   

职业接触拟除虫菊酯工人精子浓度的调查

目的调查拟除虫菊酯暴露与工人体内氧化应激状态和精子浓度的关联性,为制定拟除虫菊酯职业暴露引起男性职业性生殖毒性损害的诊断标准提供依据。方法2020年9—10月,选取武汉市某拟除虫菊酯类农药工厂一线岗位234名成年男性工人为暴露组,117名成年男性行政后勤人员为对照组,收集调查对象的一般人口学信息并采集尿液5 mL,检测尿中3-苯氧基苯甲酸(3-PBA)、8-羟氧基苯甲酸(8-OHdG)浓度;采集调查对象禁欲3 d后的精液,测量精子浓度。同时检测该工厂生产工人主要接触的化学有害因素浓度。结果生产工人主要接触的化学有害因素为:溴氰菊酯、氯氰菊酯、高效氯氰菊酯和顺式氯氰菊酯。暴露组人员的3-PBA浓度、8-OHdG浓度均高于对照组,精子浓度低于对照组,差异均有统计学意义(P<0.01)。经Person相关性检验,351名研究对象3-PBA浓度与8-OHdG浓度呈正相关(r=0.511,P<0.01),与精子浓度呈负相关(r=-0.546,P<0.01);8-OHdG浓度(经自然对数转换)与精子浓度呈负相关(r=-0.113,P<0.05)。线性回归模型分析结果显示:(1)尿中3-PBA浓度(经自然对数转换)每增加1μg/g,8-OHdG浓度增加7.362μg/g,精子浓度减少0.136×10^(8)个/mL;(2)BMI每增加1 kg/m2,8-OHdG浓度增加0.396μg/g,精子浓度减少0.014×10^(8)个/mL。未观察到年龄、吸烟、饮酒与8-OHdG浓度、精子浓度之间的剂量-效应关系。结论拟除虫菊酯暴露可能会升高男性职业接触人群氧化应激水平,降低精子浓度,应加强工人的职业防护。     

Oxidative DNA damage estimated by urinary 8-hydroxydeoxyguanosine and indoor air pollution among non-smoking office employees

This study investigated whether urinary 8-hydroxydeoxyguanosine (8-OHdG), a biomarker of oxidative stress, was associated with indoor air quality for non-smokers in high-rise building offices. With informed consents, urine samples from 344 non-smoking employees in 86 offices were collected to determine 8-OHdG concentrations. The concentrations of carbon dioxide (CO(2)) and total volatile organic compounds (TVOCs) in each office and outside of the building were simultaneously measured for eight office hours. The average workday difference between indoor and outdoor CO(2) concentrations (dCO(2)) was used as a surrogate measure of the ventilation efficiency for each office unit. The CO(2) levels in the offices ranged 467-2810ppm with a mean of 1170ppm, or 2.7 times higher than that in the outside air. The average urinary 8-OHdG levels among employees increased from 3.10 micro g/g creatinine, for those at the lowest tertile levels of both dCO(2) and TVOCs, to 6.27 micro g/g creatinine, for those at the highest tertile levels. Multivariate logistic regression analysis showed that the risk of having the urinary 8-OHdG level of greater than the median, 4.53 micro g/g creatinine, for participants was increased significantly at the highest tertile dCO(2) level of >680ppm (odds ratio (OR)=3.37, 95% confidence interval (CI)=1.20-9.46). The effect was significant at the middle tertile TVOCs level of 114-360ppb (OR=2.62, 95% CI=1.43-4.79), but not at the highest tertile. Inadequate ventilation in office increases the risk of building-related oxidative stress in non-smoking employees.     

吸烟和年龄对电子垃圾拆解工人尿液中8-羟基脱氧鸟苷的影响

目的 研究吸烟和年龄对电子垃圾拆解工人尿液中8-羟基脱氧鸟苷(8-hydroxy-2'-deoxyguanosine,8-OHdG)的影响.方法 采用固相萃取-高效液相色谱电化学检测器(SPE-HPLC-ECD)方法,检测64名电子垃圾拆解男性工人上班前和下班后尿液中8-OHdG浓度.按照吸烟情况和工人的年龄分别对数据进行统计分析.结果 相对于吸烟者(42名),不吸烟者(22名)尿中8-OHdG浓度明显的增高,上班前,不吸烟组的工人尿液中的8-OHdG浓度为(8.25±4.23)μmol/mol肌酐,吸烟组工人尿液中8-OHdG浓度为(5.44±1.18)μmol/mol肌酐,两者差异无统计学意义(t=-0.81,P=0.42).而在下班后,不吸烟组的工人尿液中的8-OHdG浓度为(43.12±16.19)μmol/mol肌酐,大约是吸烟组工人尿液中8-OHdG浓度[(14.82±2.51)μmol/mol肌酐]的3倍.经过1 d暴露下班后,吸烟和不吸烟工人尿液中的8-OHdG浓度差异具有统计学意义(t=-2.33,P<0.05).按照工人的年龄分组,上班前,19岁～(6名)、20岁～(22名)、30岁～(23名)、40～49岁(11名)组工人尿中8-OHdG浓度分别为(1.86±0.66)、(3.57±0.54)、(8.12±4.10)、(11.39±3.70)μmol/mol肌酐,组间差异没有统计学意义(F=0.98,P=0.41);但经过1 d的暴露,下班后,19岁～、20岁～、30岁～、40～49岁组工人尿中8-OHdG浓度分别为(4.19±2.85)、(19.89±5.26)、(28.89±14.61)、(34.94±12.50)μmol/mol肌酐,组间差异具有统计学意义(F=4.81,P=0.03).结论 吸烟对拆解工人尿中8-OHdG浓度有一定的抑制作用,尿中8-OHdG浓度随年龄增高而增加.     

Rapid and intermediate N-acetylators are less susceptible to oxidative damage among 4,4′-methylenebis(2-chloroaniline) (MBOCA)-exposed workers

Objectives

In this study, we explored the association between a marker of oxidative stress, 8-hydroxydeoxyguanosine (8-OHdG), and genetic polymorphism of the carcinogen-metabolizing enzyme N-acetyltransferase 2 (NAT2) among 4,4′-methylenebis(2-chloroaniline) (MBOCA)-exposed workers.

Methods

The study population was recruited from four MBOCA-producing factories, and included 57 MBOCA-exposed workers and 101 unexposed control workers. Personal characteristics were collected by questionnaire. Plasma 8-OHdG levels were measured by LC/MS/MS. NAT2 alleles were measured by polymerase chain reaction-based restriction fragment length polymorphism (PCR-RFLP).

Results

NAT2 polymorphism influenced the plasma 8-OHdG levels of MBOCA-exposed workers, but not of non-exposed workers. No difference between exposed and control groups was found for the crude 8-OHdG levels among rapid, intermediate, and slow acetylators. After adjusting for gender, age, smoking, and alcohol consumption habit, the 8-OHdG concentration in the MBOCA-exposed workers was 0.18 pg/ml (95% CI −1.80 to −0.12) lower than the control group among rapid and intermediate acetylators. However, the difference between exposed and control groups was not significant for slow acetylators.

Conclusion

Gene–environment interactions could play a role in the carcinogenesis of occupational MBOCA exposure. We suggest that the impact of the NAT2 acetylator status is low, if at all, on the generation of the oxidative stress marker 8-OHdG in the investigated exposed group.     

Urinary 8-hydroxydeoxyguanosine as a biomarker of oxidative DNA damage in workers exposed to ethylbenzene

This study assessed the relationships between ethylbenzene exposure and levels of 8-hydroxydeoxyguanosine (8-OHdG) among spray painters. Sixty-four male workers employed at a large shipyard were recruited for this investigation. Fifteen spray painters exposed to paint, together with two non-exposed groups, namely 19 sandblasting workers and 30 office staffs were selected as the subjects. Personal exposure to xylene and ethylbenzene in air were collected using diffusive samplers. Urine samples of the spray painters were collected after a month-long holiday leave and during the pre- and post-workshifts. Urine samples of sandblasting workers and office staffs were gathered after their shift. Urinary mandelic acid and methyl hippuric acid were used as biological indices of dose of ethylbenzene and xylene, respectively. Urinary 8-OHdG was used as biomarker of oxidative DNA damage. The post-workshift concentration of urinary 8-OHdG for 10 spray painters (30.3 ± 9.28 μg g(-1) creatinine) significantly exceeded that of holiday leave (7.20 ± 1.08 μg g(-1) creatinine; P = 0.001). The post-workshift concentration of urinary 8-OHdG was higher among 15 spray painters (29.0 ± 6.52 μg g(-1) creatinine) than sandblasting workers (9.14 ± 2.05 μg g(-1) creatinine; P = 0.01) and office staffs (8.35 ± 0.84 μg g(-1) creatinine; P = 0.007). A stepwise regression model revealed an 8.11 μg g(-1) creatinine increase per 1 p.p.m. increase in ethylbenzene [95% confidence interval (CI) 4.13-12.1]. A stepwise regression model revealed an increase of 6.04 μg g(-1) creatinine (95% CI 2.23-9.84) per 1 p.p.m. in ethylbenzene after adjustment of age (95% CI 2.23-9.84). This pilot study suggests that occupational exposure to paint increases oxidative DNA injury. Moreover, urinary 8-OHdG levels displayed greater DNA damage in spray painters compared to other unexposed groups and their holiday leave samples. A significant correlation was found between urinary 8-OHdG and the exposure to ethylbenzene. The ethylbenzene exposure could not explain all urinary 8-OHdG measured. Other components of paint deserve further investigation.     

某电网企业职工职业紧张与抑郁症状的关联研究

  目的  了解某电网企业职工职业紧张与抑郁症状的现况及相关性,探究抑郁症状的影响因素。
  方法  选择某电网企业1 091名职工为研究对象,采用工作内容问卷（JCQ）和付出-回报失衡问卷（ERIQ）测量职业紧张情况,采用中文版流行病学研究中心用抑郁量表（CES-D）调查职工抑郁症状。采用多因素logistic回归分析抑郁症状的影响因素。
  结果  共有974名（占89.3%）工人有效完成本次调查。研究对象主要接触的职业病危害因素为噪声、电磁辐射,抑郁症状检出率为36.7%。多因素logistic回归分析结果显示:在JDC模式下,睡眠时长为6~7 h、>7 h组出现抑郁症状风险分别是 < 6 h组的0.658倍（95% CI:0.481~0.901）和0.362倍（95% CI:0.239~0.550）;视屏作业者出现抑郁症状的风险是非视屏作业者的1.493倍（95% CI:1.118~1.995）;中、高社会支持组出现抑郁症状的风险分别是低社会支持组的0.594倍（95% CI:0.430~0.821）和0.539倍（95% CI:0.342~0.850）;JDC模式高职业紧张职工出现抑郁症状的风险是低职业紧张的1.667倍（95% CI:1.239~2.242）。在ERI模式下:睡眠时长为6~7 h、> 7 h组出现抑郁症状风险分别是睡眠时长 < 6 h组的0.674倍（95% CI:0.490~0.927）和0.394倍（95% CI:0.258~0.601）;视屏作业者出现抑郁症状风险是非视屏作业者的1.475（95% CI:1.100~1.978）倍;高内在投入及EIR模式高职业紧张职工出现抑郁症状的风险分别是低内在投入及低职业紧张的1.813倍（95% CI:1.234~2.664）和2.554倍（95% CI:1.866~3.495）。
  结论  该电网企业职工抑郁症状发生率较高。企业应建设良好的工作环境,增加对职工的社会支持,缓解职业紧张程度;职工也应合理安排作息时间,采取增强自我调节能力和缓解自身工作压力等措施预防抑郁症状的发生。
     

Occupation and risk of esophageal and gastric cardia adenocarcinoma

BACKGROUND: Adenocarcinomas of the esophagus and gastric cardia have risen dramatically in incidence over the past few decades, however, little research has been conducted on the occupational risk factors for these cancers. METHODS: In this population-based case-control study, lifetime job histories were compared between cases of esophageal adenocarcinoma (n = 283), gastric cardia adenocarcinoma (n = 259), and population controls (n = 689). Odds ratios (OR) and 95% confidence intervals (CI) for ever employment and by duration in various occupational and industrial categories were calculated using unconditional logistic regression. RESULTS: The risk of esophageal adenocarcinoma was elevated for persons ever employed in administrative support (OR = 1.5; 95%CI = 1.0-2.1); financial, insurance, and real estate (OR = 1.6; 95%CI = 1.0-2.4); and health services (OR = 2.2; 95%CI = 1.2-3.9). The risk of gastric cardia adenocarcinoma was increased among transportation workers (OR = 1.7; 95%CI = 1.1-2.6), as well as among carpenters (OR = 1.8; 95%CI = 0.9-3.9) and workers in the furniture manufacturing industry (OR = 2.4; 95%CI = 0.9-6.3). However, we observed few duration-response relations between length of employment in any category and cancer risk. CONCLUSIONS: This study revealed associations of esophageal adenocarcinoma with employment in administrative support, health services, and a category of financial, insurance, and real estate industries, and of gastric cardia adenocarcinoma with transportation and certain woodworking occupations. Some of these findings may be due to the play of chance associated with the multiple comparisons made in this study. Our results suggest that, overall, workplace exposures play a minor role in the etiology and upward trend of esophageal and gastric cardia adenocarcinomas.