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电子垃圾拆解区新生儿体内重金属负荷及其对生物发育的影响
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摘要
研究背景现代科技飞速发展促使电子产品频繁地更新换代,一系列范围广泛且不断增加的电子淘汰品正以惊人的速度增长,已成为世界上增长最快的垃圾。全世界数量惊人的电子废弃物大多数出口至亚洲,这其中大部分进入中国,广东汕头贵屿镇就是世界电子废弃物终点站之一。电子废弃物又叫电子垃圾,其中含有种类繁多的有毒有害物,以重金属的危害尤为突出,如铅、镉、汞和六价铬等。如果回收处理不当,将给社会、环境、健康带来一系列严重问题,对当地环境和居民健康构成一定的威胁。贵屿镇有着近20年的电子垃圾回收拆解历史,以手工拆解为主的简单落后的处理方式已使当地环境中多种重金属的含量严重超标。而胎儿期是生长发育的关键时期,对有毒有害物质极为敏感,上述物质会对胎儿的生长发育造成极大的伤害。但迄今为止,针对电子垃圾回收拆解地区胎儿或新生儿体内重金属负荷水平的相关研究还未见报道。为此,我们以广东省汕头市贵屿镇作为研究现场,在对贵屿地区03年到07年新生儿出生情况进行调查之后,以当地新生儿为研究对象,结合母亲的问卷调查,先后2年对该镇新生儿体内的铅、镉和铬负荷状况进行监测;同时对δ氨基-γ-酮戊酸脱水酶(δ-aminolevulinic acid dehydratase, ALAD)基因多态性、胎盘金属硫蛋白(Metallothionein, MT)表达、新生儿神经行为发育和脐带血淋巴细胞DNA损伤情况进行研究,探讨环境重金属污染对新生儿生长发育的影响,综合评估不科学的电子垃圾回收拆解方式对这个人群健康的危害。
     目的调查贵屿电子垃圾回收拆解区新生儿出生情况;监测当地新生儿铅、镉和铬负荷,分析其变化趋势;探讨影响新生儿铅、镉和铬负荷的因素;初步评估当地新生儿生长发育情况,评估不科学的电子垃圾回收处理方式对新生儿生长发育的影响。
     方法首先采用回顾性调查的方式,以厦门妇幼保健院数据为对照组调查2003~2007年贵屿地区产妇及新生儿的生育和出生情况。其次以贵屿镇当地医院妇产科出生新生儿为暴露组研究对象,以潮南民生医院妇产科出生新生儿为对照组,采用石墨炉原子吸收光谱法,分别对贵屿镇2006年及2007年当地出生新生儿脐带血铅、胎粪铅、脐带血镉、胎盘镉和脐带血铬水平进行监测,并以问卷形式对新生儿父母的家庭和工作环境状况进行调查。以限制性片段长度多态性(Restriction fragment length polymorphism, RFLP)方法对新生儿ALAD基因型进行分析,采用链霉菌素-生物素(S-P)免疫组化技术检测新生儿胎盘MT的表达,采用国际认可的鲍秀兰20项新生儿神经行为检查法对新生儿神经行为能力评分,用彗星实验检测新生儿脐带血淋巴细胞DNA的损伤情况。
     结果1.调查数据显示从03年到07年及5年总和死胎率贵屿组明显高于厦门对照组。早产率除05年数据厦门组略高于贵屿组外,其它03年、04年、06年、07年、5年总和均为贵屿组高于厦门组。低体重儿发生率03年到07年及5年总和均为贵屿组高于厦门组。双胎率03年、04年、05年、07年、5年总和为贵屿组高于厦门组,而06年为厦门组高于贵屿组。05年死胎率、06年低体重儿发生率、除04年外的双胎率差异无统计学意义(χ2检验,P >0.05),其余所有差异均有统计学意义(χ2检验,P<0.05)。03到07年每年总异常出生情况均为贵屿组高于厦门组,05年差异无统计学意义(χ2检验,P >0.05),其余每年差异均有统计学意义(χ2检验,P<0.05)。
     2.1)2006年贵屿地区新生儿脐带血铅值(均数为113.28μg/L)明显高于贵屿周边其它乡镇(平均值为60.43μg/L),差别具有统计学意义(P <0.01)。超过目前认为的安全临界线(100μg/L)者48例,占该组的48%。2007年贵屿地区新生儿脐带血铅值(均数为110.86μg/L)也明显高于贵屿周边其它乡镇(平均值为53.38μg/L),差别具有统计学意义(P <0.01)。超过目前认为的安全临界线(100μg/L)者59例,占该组的59%。2007年贵屿组脐带血铅均值低于2006年,但两组铅水平分布无显著性差异(P >0.05)。2006年贵屿地区新生儿胎粪铅值均数为2.50μg/g,明显高于贵屿周边其它乡镇新生儿胎粪铅值(均数为1.20μg/g),差别具有统计学意义(P<0.01)。2007年因取材原因无对照组数据,贵屿实验组新生儿胎粪铅均数为4.54μg/g。贵屿地区2007年胎粪铅值高于2006年,分布有显著性差异(P<0.01)。父母从事电子垃圾相关工作、在贵屿居住时间等是导致贵屿地区新生儿高铅负荷的相关因素。
     2)2006年贵屿组新生儿脐带血镉均值为5.30μg/L,超标率为29%;2007年均值3.47μg/L,超标率为10 %,两年均值和超标率均高于同年对照组(P<0.01)。并且贵屿组2007年均值与超标率均低于2006年,差异具有统计学意义(P <0.01)。2006年实验组新生儿胎盘镉均值为0.17μg/g,明显高于对照组(0.10μg/g),差异具有统计学意义(P<0.01)。父母从事电子垃圾相关工作、在贵屿居住时间等是导致贵屿地区新生儿高镉负荷的相关因素。
     3)贵屿实验组2006年脐带血铬水平(均值为303.38μg/L,中位数93.89μg/L),超过目前认为相对安全界限(0.20μg/L)为29例,超标率29%;对照组脐带血铬水平(均数20.30μg/L,中位数18.10μg/L)均未超过目前认为的相对安全界限;无论是铬的超标率还是均值及中位数,贵屿实验组和对照组比较,差别均有统计学意义(P<0.01)。2007实验组年脐带血铬水平(均值为99.90μg/L,中位数70.60μg/L ),超过目前认为相对安全界限为9例,超标率9%;对照组脐带血铬水平(均数32.48μg/L,中位数24.00μg/L)均未超过目前认为的相对安全界限。2007年铬的超标率和均值及中位数,贵屿实验组和对照组比较,差别同样有统计学意义。贵屿实验组06年与07年脐带血铬均值和超标率差别均无统计学意义(P > 0.05)。父母从事电子垃圾相关工作、在贵屿居住时间等是导致贵屿地区新生儿高铅负荷的相关因素。
     新生儿脐带血铅、镉和铬水平具有正相关性。
     3.铅易感基因ALAD在电子垃圾拆解区新生儿中存在多态性。在全国范围内,当地新生儿的铅易感等位基因ALAD2的分布频率处于较低水平。本研究未发现ALAD基因型与新生儿脐带血铅水平有相关性。
     4.贵屿实验组100例胎盘中有67例MT呈阳性表达,阳性率为67%;对照组52例胎盘中MT呈阳性表达的为17例,阳性率为32.69 %,实验组阳性表达率明显高于对照组(P< 0.01)。胎盘MT的表达量与新生儿脐带血镉水平及胎盘镉水平具有显著相关性。
     5.贵屿实验组与对照组新生儿各项评分t检验比较,新生儿神经行为总评分、直立反射、行为能力、非生物视定向反应评分具有显著性差异(P <0.05),主动肌张力、牵拉反射、非生物听定向反应、生物视听定向反应评分无显著性差异(P >0.05)。胎粪铅值与新生儿行为神经评估得分、主动肌张力、行为能力、牵拉反射、直立反射、非生物听定向反应、非生物视定向反应、生物视听定向反应有显著负相关性,脐带血铅值与它们没有相关性。新生儿神经行为总评分与脐带血镉和铬水平都有负相关性,行为能力与镉水平有负相关性,非生物视定向反应与铬水平有负相关性。
     6.贵屿地区新生儿脐带血淋巴细胞DNA损伤情况(拖尾率和彗星细胞尾长)明显高于对照组,差异有统计学意义(P <0.05)。新生儿脐带血铬水平与拖尾率即彗星细胞数和彗星细胞尾长成正相关。脐带血镉与拖尾率成正相关,与彗星细胞尾长无相关性。脐带血铅与拖尾率和彗星细胞尾长均无相关性。
     结论电子垃圾拆解区新生儿异常出生率处于较高水平。部分新生儿处于高铅、高镉和高铬负荷状态,整体看07年新生儿镉和铬负荷值较06年有所下降,但从全国平均水平来看仍处于高水平状态;父母从事电子垃圾回收工作、父母在贵屿居住时间等是影响新生儿铅、镉和铬负荷的因素。从遗传特质上来讲,该地新生儿对铅的遗传易感性低于国内外水平,且ALAD基因型未见与贵屿镇新生儿的脐带血铅水平有相关性,在此遗传特性下,该地区的新生儿血铅水平依然处于较高水平,间接地说明了该镇电子垃圾的不规范处理方式造成的环境污染已对新生儿健康构成威胁。镉暴露后机体被诱导产生更多的MT是机体重要的防护机制之一,同时MT水平随镉暴露量而变化。本实验通过对胎盘MT表达量的检测进一步提示在贵屿地区镉的污染现实,以及胎盘对镉暴露反应的灵敏性,排除内在因素对新生儿镉水平的影响,环境是新生儿镉水平超标的主要因素。通过对新生儿神经行为评估提示贵屿地区的铅、镉和铬暴露可能会影响新生儿神经行为发育,对新生儿今后中枢神经系统尤其是智能发育可能会有不良影响。新生儿脐带血淋巴细胞DNA损伤情况提示贵屿地区铬、镉污染状况有可能已经危及到新生儿的生长发育状况,有可能导致当地新生人口质量的下降,如果不加以重视,未来可能会有严重的后果。
Background The rapid development of modern science and technology accelerates the generation of new electronic products. In the meantime, the obsoleted electronic products are increasing at an astonishing rate, and have become the world's largest source of electronic wastes. Most of these electronic wastes enter Asia, most of which are sent to China. Guiyu, a town in Guangong Province, is one of the destinations of the electronic wastes. These electronic wastes contain variety of poisonous hazard. The most harmful substances are heavy metals such as Lead, Cadmium, Mercury, Chromium and the etc. These substances cause serious problems to the society, environment, and public health if recycled not properly. Guiyu has more than 10 year history of electronic wastes recycling. The primary process method is manually handling and disassembling. This primitive and uncontrolled method spreads harmful substance to the surroundings. As a result, the heavy metal levels in local environment had far exceeded regulation. As we all known, embryo stage is the most critical time in human life development. The embryo is vulnerable to hazardous substances especially, to those mentioned above. However, there is no report on studies about heavy metal levels inside newborns in the electronic waste recycle regions. Therefore, we took Guiyu town of Guangdong Province as investigation site and, Guiyu local newborns as study object, collected surveys from mothers of these infants, and spent two yeas of investigations to local newborns regarding the levels of Lead, Cadmium and Chromium in their bodies. In the meantime, we studied nerve behavior development; the ALAD gene polymorphism, the placenta metallothionein expression, and the umbilical cord blood lymphocyte DNA damage situation; discussed the effect of heavy metal pollution to the newborns' growth and development; and assessed the harmfulness of unscientific electronic waste recycling to the public health of this region.
     Objective To investigate the abnormal birth rate of newborns in Guiyu. To explore the load condition of Lead, Cadmium and Chromium, the trend of its changes, and its relation to newborns' growth and development in electronic wastes recycling area. To assess the harmful effect to public health due to unscientific electronic waste recycle.
     Methods First investigates Guiyu area lying-in women and newborns' birth situation from 2003 to 2007 by reviewing available records. Next take the newborns from Guiyu local hospital as the research objects, categorized as Exposure Group; take those born from Chaonan Minsheng Hospital, categorized as Control Group. Utilize the atomic absorption spectrophotometry methods to monitor in 2006 and in 2007, umbilical cord blood Lead levels, meconium Lead levels, umbilical cord blood Cadmium levels, placenta Cadmium levels, umbilical cord blood Chromium levels of newborns; and survey in the form of question and answer to the family and working conditions of the newborns' parents. Apply the international approval BaoXiulan 20 items of newborns neonatal behavioral neurological assessment to grade the newborns' nerve behavioral capability. Apply Restriction fragment length polymorphism (RFLP) method to analyze ALAD gene. Use S-P immunity histochemistry technology to examine placenta metallothionein expression. Use the The Comet Experiment to examine newborns' umbilical cord blood lymphocyte DNA damage situation.
     Results 1. Comparison of Guiyu Group to Xiamen Group Data indicated that Guiyu Group had significant higher still death rate than Xiamen Group did each year from 2003 to 2007 as well as the totals of 2003 to 2007. Guiyu Group had higher premature delivery rate than Xiamen Group did each year from 2003 to 2007 as well as the totals of 2003 to 2007 except in 2005. Guiyu Group had higher low body weight rate than Xiamen Group did each year from 2003 to 2007 as well as the totals from 2003 to 2007. Guiyu Group had higher twin rate than Xiamen Group did each year from 2003 to 2007 but lower in 2006. The total twin rate from 2003 to 2007 was higher in Guiyu Group.
     2. 1) In 2006 the Guiyu area newborns umbilical cord blood Lead levels (mean: 113.28μg/L) was significantly higher than its neighboring towns (mean value: 60.43μg/L). The difference had statistics significance (P < 0.01). 48 occurrence exceeded current known safety guideline (100μg/L), counting 48% of this group. In 2007 the Guiyu area newborns umbilical cord blood Lead levels (mean: 110.86μg/L) was significantly higher than its neighboring towns (mean: 53.38μg/L). The difference had statistics significance (P < 0.01). 59 occurrences exceeded present safety guideline (100μg/L), counting 59% of this group. In 2007 the Guiyu group umbilical cord blood Lead mean was lower than what in 2006, but the two lead levels distribution did not have significant difference (P > 0.05).
     In 2006 the Guiyu area newborns meconium lead levels mean was 2.501μg/g, significantly higher than its neighboring towns meconium Lead levels (mean: 1.200μg/g). The difference had statistics significance (P < 0.01). In 2007 the Guiyu newborns meconium Lead levels mean was 4.54μg/g. However, in 2007 meconium the lead levels were higher than in 2006. The distribution had significant difference (P < 0.01). Parents' Engaging with the electronic wastes recycle, living in this area and the length of living in this area were factors of high lead load newborns.
     2) In 2006 the Guiyu group had umbilical cord blood Cadmium mean of 5.30μg/L, exceed rate was 20%. In 2007 the mean was 3.47μg/L, exceeding rate was 10%. Both Guiyu two years mean and exceeding rates were higher than those in the same year in Control Group (P < 0.01). In addition, both mean and exceeding rate of Guiyu Group in 2007 were lower than what in 2006, the difference had statistics significance (P < 0.01). In 2006 Guiyu Group newborns placenta Cadmium mean was 0.17μg/g, much higher than Control Group (0.10μg/g). The difference had statistics significance (P< 0.01). Parents' Engaging with the electronic wastes recycle, living in this area and the length of living in this area were factors of high Cadmium load newborns.
     3) Umbilical cord blood Chromium levels in 2006, Guiyu Group's levels (mean: 303.38μg/L, median: 93.89μg/L) had 29 occurrences exceeding current acceptable safe limit (0.20μg/L), exceeding rate 29%. Control Groups' levels (mean: 20.30μg/L, median: 18.10μg/L) was within current acceptable safe limit. Comparing Guiyu Group and Control Group, the difference had statistics significance either in the exceeding rate or in the mean. Umbilical cord blood Chromium levels in 2007, Guiyu Group's levels (mean: 99.90μg/L, median: 70.60μg/L) was higher than current acceptable safe limit: 9 occurrences, exceeding rate 9%. Control Group's levels (mean: 32.48μg/L, median: 24.00μg/L) was within current acceptable safe limit. Comparing Guiyu Group and Control Group, the Chromium exceeding rate and the mean, the differences had statistics significance. The differences of Guiyu Group umbilical cord blood Chromium mean and exceeding rate between 2006 and 2007 had no statistic significance (P > 0.05). There were positive correlations were found between umbilical cord blood Lead levels and Cadmium levels and Chromium levels.
     3. Lead sensitivity gene ALAD of newborns in electronic waste recycle area had various statuses. Nationwidely, the frequency of local newborns Lead sensitivity gene ALAD2 was at relatively low levels. This research so far had not discovered ALAD gene type correlation with newborns umbilical cord blood Lead levels.
     4. There were 67 placenta samples metallothionein of 100 totals in Guiyu Group, showing positive expression, positive rate 67%. There were 17 placenta samples metallothionein of 57 totals in Control Group, showing positive, positive rate 32.69%. Guiyu Group had much higher positive rate (P < 0.01).
     The placenta metallothionein expression quantity had positive correlation with umbilical cord blood Cadmium level and placenta Cadmium level of newborns.
     5. Comparison all subjects (t test) between Guiyu Group and Control Group. Guiyu Group neonatal behavioral neurological total scores, stands still reflection, behavioral capability, and non-biology vision directional responses had significant difference (P < 0.05). The initiative myo-tensity, pulls the reflection, non- biology directional hearing response, biological directional vision and hearing responded did not have significant difference (P > 0.05). Meconium Lead value had remarkable negative correlation with newborn behavior nerve assessment, initiative myo- tensity, behave capability, lead-pull reflection, stand still reflection, non- biology directional hearing response, non- biology directional vision response, and biological directional hearing and vision response had remarkable. However, the umbilical cord blood Lead value did not have correlation with them. Cord blood Cadmium and Chrome levels had negative correlation with newborn behavior nerve assessment. Core blood Cadmium levels had negative correlation with behave capability. Cord blood Chrome levels had negative correlation wirh non-biology directional vision response.
     6. There were remarkable differences (P < 0.05) of tailing rate and tail long between Guiyu Group and Control Group. In addition, there was correlation between DNA damage and umbilical cord blood Chromium and Cadmium levels of newborns.
     Conclusion The abnormal birth rate of neonates in Guiyu was at a relatively high level. A portion of newborns in electronic waste recycle area were in high Lead, high Cadmium, and high Chromium load condition. Although newborns in 2007 had lower Cadmium, and Chromium load levels than in 2006, but still at high level compared with national average. Parents' Engaging with the electronic waste recycle, living in Guiyu area and the length of living in this area were influencing factors of Lead, Cadmium, and Chromium load on newborns. From genetic characteristics view, local newborns were less susceptible to Lead in heredity, and there was no seen relevance of ALAD gene with Guiyu newborns umbilical cord blood Lead levels. But Guiyu newborns blood Lead levels were still at high level. This fact indirectly explained that the environmental pollution due to unregulated electronic waste recycle in Guiyu is threatening local newborns' health. Human body will produce more MT when induced by Cadmium exposed in the environment, which is one of the important human body self protection mechanisms. The MT level varies with the quantity of Cadmium in the environment. Through examining the quantity of placenta MT, this research further reveals the fact of pollution in Guiyu area, and the sensitivity of placenta to the Cadmium exposed in environment. Excluding internal factor influence to newborn Cadmium levels, environment is the primary factor that causes newborn Cadmium levels higher than acceptable level. Through neonatal behavioral neurological assessment, this research alerts that the Lead/Cadmium/Chrome exposure in Guiyu area will possibly affect the growth of newborn nerve behavior. It will potentially hinder the development of newborns central nerve system particularly, the development of their intelligence. Umbilical cord blood lymphocyte DNA of newborns damage situation alerts that Guiyu area Chromium and Cadmium pollution perhaps already endangered newborns' health, which can lower the quality of local new population. It will possibly lead to serious consequence if we do not pay enough attention to the pollution in the environment now.
引文
1. Dirk B. Electronic scrap: a growing resource. Precious Metals. 2001, (7): 21-24.
    2. The Basel Action Network (BAN). Silicon Valley Toxics Coalition (SVTC). Exporting harm: the high-tech wasteing of Asia. 2002.
    3.张敦信,吕峰.废旧电脑的环境污染与防治.城市管理与科技. 2004, 6(1): 28-31.
    4.刘助仁.迎接电子垃圾的挑战.再生资源研究. 2004, (4): 6-8.
    5. NO authors listed. Climbing the e-waste mountain. J Environ Monit. 2005, 7(10): 933-936.
    6. Christen K. U.S. rules could increase e-waste exports. Environ Sci Technol. 2002, 36(15): 309-310.
    7.郑会侠.靠垃圾发财靠环保兴家.源流. 2007, 5: 14-15.
    8.白玲.贵屿电子垃圾第一镇.文明. 2007, 5: 114-128.
    9.陈宇辉.贵屿电子垃圾无间道.明白风尚(生活态度). 2007, 2: 14-19.
    10.刘阳乾.贵屿电子垃圾拆解业发展原因分析.特区经济. 2006, 10: 357-358.
    11. Sclunidt CW. Unfair trade: e-waste in Africa. Environ Health Perspect. 2006, 114(4): 232-235.
    12.贵屿建大型电子电器交易市场.有色金属再生与利用. 2006, 11: 12.
    13.贵屿-富蔗的垃圾城.绿叶. 2005, 1.
    14.刘辉.电子垃圾中的孤岛—贵屿能否重生.资源与人居环境. 2007, 19: 56-57.
    15.赖云.贵屿故事:记一电子废物拆解地.资源与人居环境. 2006, 7: 44-49.
    16. Wang JP, Guo XK. Impact of electronic wastes recycling on environmental quality. Biomed Environ Sci. 2006, 19 (2): 137-142.
    17.黄慧诚.贵屿的教训.环境. 2002, 4: 18-19.
    18.王灏.透视贵屿.电器. 2004, 5: 22-24.
    19. Wong CS, Wu SC, Duzgoren-Aydin NS, Aydin A, Wong MH. Trace metal contamination of sediments in an e-waste processing village in China. Environ Pollut. 2007, 145(2): 434-442.
    20. Wong MH, Wu SC, Deng WJ, Luo Q, Leung AQ, Wong CS, Luksemburg WJ, Wong AS. Export of toxic chemicals-a review of the case of uncontrolled electronic-waste recycling. Environ Pollut. 2007, 149(2): 131-140.
    21. Wong CS, Duzgoren-Aydin NS, Aydin A, Wong MH. Evidence of excessive releases of metals from primitive e-waste processing in Guiyu, China. Environ Pollut. 2007, 148(1): 62-72.
    22.王攀.贵屿镇:电子垃圾的“绿色梦想”.中国信息界. 2005, 8: 21-22.
    23.陈燕璇.从潮阳贵屿废旧电子污染看我国环境成本.环境. 2006, S2: 66-68.
    24.林俊生.贵屿:电子垃圾城的重生.环境经济杂志. 2005, 4: 19-22.
    25.钟再训.广东贵屿废旧回收行业在整治中发展.有色金属再生和利用. 2005, 3: 20-25.
    26.王扶笠.对电子垃圾污染治理的思考和对策.陕西环境. 2003, 10(6): 62-64.
    27.温学新.环境因素与肺癌关系研究进展.交通大学. 2000, 14(5): 457-458.
    28. Jang YC, Townsend TG. Leaching of lead from computer printed wire boards and cathode ray tubes by municipal solid waste landfill leachates. Environ Sci Technol. 2003, 37(20): 4778-84.
    29. Kang HY, Schoenung JM. Economic analysis of electronic waste recycling: modeling the cost and revenue of a materials recovery facility in California. Environ Sci Technol. 2006, 40(5): 1672-80.
    30. Macauley M, Palmer K, Shih JS. Dealing with electronic waste: modeling the costs and environmental benefits of computer monitor sisposal. Environ Manage. 2003, 68(1): 13-22.
    1. Brigden K, Labunska I, Santillo D, et al. Recycling of electronic wastes in China and India: workplace and environmental contamination. 2005 Available:http://www.greenpeace.org/india/press/reports/recycling-of-electronic-wastes.
    2. Wong CS, Wu SC, Duzgoren-Avdin NS, Avdin A, Wong MH. Trace metal contamination of sediments in an e-waste processing village in China. Environmental Pollution. 2007, 145(2) 434-442.
    3.丘波,彭琳,徐锡金,林歆胜,林哲睿,洪继丹,郭洪创,霍霞.电子废弃物回收拆解业工人健康调查.环境与健康杂志. 2005, 22(6): 419~421.
    4.韩岱,霍霞,郑良楷,李燕.电子废物拆解区儿童血铅和智力情况调查.汕头大学医学院学报. 2007, 20(3): 170-172.
    5. Bell ML, Ebisu K, Belanger K. Ambient Air Pollution and Low Birth Weight in Connecticut and Massachusetts. Environmental Health Perspectives. 2007, 115(7): 1118-1124.
    6. Huo X, Peng L, Xu XJ, Zheng LK, Qiu B, Qi ZL, Zhang B, Han D, Piao ZX. Elevated Blood Lead Levels of Children in Guiyu, an Electronic Waste Recycling Town in China. Environmental Health Perspectives. 2007, 115(7): 1113-1117.
    7. Wong CS, Duzgoren-Aydin NS, Aydin A, Wong MH. Evidence of excessive releases of metals from primitive e-waste processing in Guiyu, China. Environ Pollut. 2007, 148(1): 62-72.
    8. Mueller BA, Kuehn CM, Shapiro-Mendoza CK, Tomashek KM. Fetal Deaths and Proximity to Hazardous Waste Sites in Washington State. Environmental Health Perspectives. 2007, 115(5): 776-780.
    9.徐锡金,丘波,李燕,朴仲贤,霍霞.电子垃圾拆解区新生儿脐带血铅水平.南方医科大学学报.(录用)
    1. Fewtrell LJ, Pruss-Ustun A, Landrigan P, Avuso-Mateos JL. Estimating the global burden of disease of mild mental retardation and cardiovascular diseases from environmental lead exposure. Environ Res. 2004, 94(2): 120-133.
    2. Raghunath R, Tripathi RM, Sastry VN, Krishnamoorthy TM. Heavy metals in maternal and cord blood.Sci Total Environ. 2000, 250(1-3): 135-141.
    3. Butler WJ, Housemans J, Seddon L, McMullen E, Tofflemire K, Mills C, Corriveau A, Weber JP, LeBlanc A, Walker M, Donaldson SG, Van Oostdam J. Maternal and umbilical cord blood levels of mercury, lead, cadmium, and essential trace elements in Arctic Canada. Environ Res. 2006, 100(3): 295-318.
    4. Harville EW, Hertz-Picciotto I, Schramm M, Watt-Morse M, Chantala K, Osterloh J, Parsons PJ, Rogan W. Factors influencing the difference between maternal and cord blood lead. Occup Environ Med. 2005, 62(4): 263-269.
    5. Emory E, Pattillo R, Archibold E, Bayorh M, Sung F. Neurobehavioral effects of low level lead exposure in human neonates. Am J Obstet Gynecol. 1999, 181(1): S2-11.
    6. Ye Ping, Liu Xiao-xian, Ke Fu-rong, Li Yan-shu, Peng Liang-bin. Relationship between neonatal neurobehavioral development and lead level in umbilical cord blood and meconium.Chinese Jounal of Clinical Rehabilitation. 2005, 9(47): 190~192.
    7.张源,罗文鸿,李慧,沈忠英. GFAAS测定氧化砷处理移植性食管癌大鼠后各组织的砷浓度.光谱学与光谱分析. 2004, 24(4): 487-490.
    8.张源,林哲绚,李慧,罗文鸿.微酸消化-石墨炉原子吸收光谱法测定大鼠组织中的钴.分析化学研究报告. 2004, 32(11): 1421-1425.
    9. Preventing lead poisoning in young children: a statement by the Centers for Disease Control. Centers for Disease Control. 1991.
    10. Centers for Disease Control. Preventing in Lead Poisoning in Young Children: A statement from the Centers for Disease control.Atlanta. GA: Centers for Disease Control, 1991: 1-74.
    11. Koller K, Brown T, Spurgeon A, Levy L. Recent developments in low-level lead exposure and intellectual impairment in children. Environ Health Perspect. 2004, 112(9): 987-994.
    12. Emory E, Ansari Z, Pattillo R, Archibold E, Chevalier J. Maternal Blood Lead Effects on Infant Intelligence at Age 7 months. Am J Obstet Gynecol. 2003, 188(4): S26-32.
    13. Ye Ping, Liu Xiao-xian, Ke Fu-rong, Li Yan-shu, Peng Liang-bin. Relationship between neonatal neurobehavioral development and lead level in umbilical cord blood and meconium. Chinese Jounal of Clinical Rehabilitation. 2005, 9(47): 190~192.
    14.颜崇淮,沈晓明,敖黎明等.上海市新生儿脐带血血铅水平及其影响因素.中华预防医学杂. 1997, 31(1): 9-12.
    15.沈彤,朱中平,俞翠莲等.婴幼儿血铅水平与出生前后铅暴露关系的队列研究.中国儿童保健杂志. 2005, 13(2): 103-105.
    16.赵文利,孔祥英,刘力建.重庆市区新生儿及其生母血铅测定及影响因素调查.重庆医学. 2001, 30(6): 514-516.
    17.宋玫,李少云,张红忠等.珠海地区胎儿铅暴露状况及其影响因素的探讨.中国优生与遗传杂志. 2002, 10(2): 72/48.
    18.幺宏彦,黄醒华.孕妇血铅水平测定及对妊娠结局的影响.中华妇产科杂志. 2003, 38(6):340-342.
    19.闫萍,霍琰,王树松等.脐带血铅水平与血钙锌的关系研究.微量元素与健康研究. 2005, 22(3): 20-24.
    20.薛向阳,贾卉,李芳等.产妇脐带血、静脉血微量元素的含量分析.中国优生与遗传杂志. 2005, 13(7): 73-74.
    21.戴伏英,范淑兰,岳晓燕等.太原市重工业区新生儿血铅及神经发育状况.中国学校卫生. 2004, 25(6): 729-730.
    22. Zentner LE, Rondo PH, Mastroeni SS. Lead contamination and anthropometry of the newborn baby. J Trop Pediatr. 2006, 52(2): 369-371.
    23. Butler Walker J, Houseman J, Seddon L, McMullen E, Tofflemire K, Mills C, Corriveau A, Weber JP, LeBlanc A, Walker M, Donaldson SG, Van Oostdam J. Maternal and umbilical cord blood levels of mercury, lead, cadmium, and essential trace elements in Arctic Canada. Environ Res. 2006, 100(3): 295-318.
    24. Kirel B, Aksit MA, Bulut H. Blood lead levels of maternal-cord pairs, children and adults who live in a central urban area in Turkey. Turk J Pediatr. 2005, 47(2): 125-131.
    25. Levesque B, Duchesne JF, Gariepy C, Rhainds M, Dumas P, Scheuhammer AM, Proulx JF, Déry S, Muckle G, Dallaire F, Dewailly E. Monitoring of umbilical cord blood lead levels and sources assessment among the Inuit. Occup Environ Med. 2003, 60(9): 693-695.
    26.杨颖.铅的神经发育毒性.国外医学卫生学分册. 2000, 27(3): 144-147.
    27. Wasserman GA, Staghezza-Jaramillo B, Shrout P, et al. The effect of lead exprosure on behavior problems in preschool chinldren. Am J Pub Heal. 1998, 88(3): 481-486.
    28. Emory E, Ansari Z, Pattillo R, Archibold E, Chevalier J. Maternal blood lead effects on infant intelligence at age 7 months. Am J Obstet Gynecol. 2003, 188(4): S26-32.
    29. Wong CS, Wu SC, Duzgoren-Aydin NS, Aydin A, Wong MH. Trace metal contamination of sediments in an e-waste processing village in China. Environmental Pollution. 2007, 145(2): 434-442.
    30. Lei XY, Xiong H. Higher blood lead levels of neonates are associated with environmental factors. Chinese Journal of Pediatrics. 2000, 38(6): 373-376.
    31.王瑛,岳书勤. 1032例新生儿及母亲血铅水平与环境因素相关性探讨.实用妇产科杂志. 2002, 18(4): 237-238.
    32. Schnaas L, Rothenberg SJ, Flores MF, Martinez S, Hernandez C, Osorio E, Velasco SR, Perroni E. Reduced Intellectual Development in Children with Prenatal Lead Exposure.Environmental Health Perspectives. 2006, 114(5): 791-797.
    33. Zentner LE, Rondo PH, Mastroeni SS. Lead contamination and anthropometry of the newborn baby. J Trop Pediatr. 2006, 52(5): 369-371.
    34. Recknor JC, Reigart JR, Darden PM, Goyer RA, Olden K, Richardson MC. Prenatal care and infant lead exposure. J Pediatr. 1997, 130(1): 123-127.
    35. Lafond J,Hamel A, Takser L, Vaillancourt C, Mergler D. Low environmental contamination by lead in pregnant women: effect on calcium transfer in human placental syncytiotrophoblasts. J Toxicol Environ Health A. 2004, 67(14): 1069-1079.
    1. Waisberg M, Joseph P, Hale B. Molecular and cellular mechanisms of cadmium carcinogenesis. Toxicology. 2003, 5(192): 95-117.
    2. Achanzar WE, AchanzarKB, Lewis JG. Cadmium induces c-myc, p53, and c-jun expression in normal human prostate epithelial cells as a prelude to apoptosis. Toxicol Appl Pharmacol. 2000, 164(3): 291-300.
    3. Matsuda T, Kobayashi E, Okubo Y, Suwazono Y, Kido T, Nishijo M, Nakagawa H, Nogawa K. Association between renal dysfunction and mortality among inhabitants in the region around the Jinzu River basin polluted by cadmium. Environ Res. 2002, 88(3): 156-163.
    4. Butler Walker J, Houseman J, Seddon L, McMullen E, Tofflemire K, Mills C, Corriveau A, Weber JP, LeBlanc A, Walker M, Donaldson SG, Van Oostdam J. Maternal and umbilical cord blood levels of mercury, lead, cadmium, and essential trace elements in Arctic Canada. Environ Res. 2006, 100(3): 295-318.
    5. Wong CS, Duzgoren-Aydin NS, Aydin A, Wong MH. Evidence of excessive releases of metals from primitive e-waste processing in Guiyu, China. Environ Pollut. 2007, 149(2): 131-140.
    6. Wong CS, Duzgoren-Aydin NS, Aydin A, Wong MH. Evidence of excessive releases of metals from primitive e-waste processing in Guiyu, China. Environ Pollut. 2007, 148(1): 62-72.
    7.孔杏云,何善元,谭小艳.新生儿血镉浓度的性别差异.湖南医科大学学报. 1999, 24(3): 305-306.
    8.赵永成,张亚利,王继先.环境镉暴露对妊娠结局和胎儿生长发育的影响.中国工业医学杂志. 2004, 17(4): 212-214.
    9.张宜明,朱圣陶,刘仁平,曹燕.苏州市部分学龄前儿童血铅、镉及红细胞游离原卟啉水平.中国学校卫生. 2003, 24(6): 601-602.
    10.付宝庆,刘青华,王成英,常纪.大庆地区4716例儿童血铅、镉水平调查分析.齐齐哈尔医学院学报. 2006, 27(2): 190.
    11.朱中平,沈彤,杨永坚等.血铅、镉等6种元素对幼儿行为问题影响的横断面研究.安徽医科大学学报. 2005, 40(6): 560-563.
    12.华莉,杨伟华,刘细珍,黄换葵,谢光雄.儿童1490例血铅、血镉水平分析.中国儿童保健杂志. 2006, 14(3): 304-305.
    13.韩光辉,卢磊,卢松丽.临沂市区学龄前儿童血铅和血镉水平调查研究.医学检验与临床. 2006, 17(2): 31-34.
    14.于青,唐子安,李芸等.济南市区239例正常女性血铅、血镉水平调查.解放军预防医学杂志. 1994, 12(5): 381-382.
    15.罗端玲.贵阳市非职业性接触人群血铅镉含量水平调查.微量元素与健康研究. 1998, 15(1): 53-54.
    16. Moon CS, Paik JM, Choi CS, Kim DH, Ikeda M. Lead and cadmium levels in daily foods, blood and urine in children and their mothers in Korea. Int Arch Occup Environ Health. 2003, 76(4): 282-288.
    17. BatáriováA, SpeváckováV, Benes B, CejchanováM, Smíd J, CernáM. Blood and urine levels of Pb, Cd and Hgin the general population of the Czech Republic and proposed reference values. Int J Hyg Environ Health. 2006, 209(4): 359-366.
    18. Schoeters G, Den Hond E, Zuurbier M, Naginiene R, Van den Hazel P, Stilianakis N, Ronchetti R, Koppe JG.. Cadmium and children: exposure and health effects. Acta Paediatr Suppl. 2006, 95(453): 50-54.
    19. Piekoszewski W, Forek E, Kornacka MK, Koroniak H, Wolny M. Level of cadmium and zinc in placenta of smoking women. Przegl Lek. 2005, 62(10): 1062-1066.
    20. Hartsfield J K J r, LeeM, Morel J G, Hilbelink DR. Statistical analysis of the effect of cadmium and zinc on hamster teratogenesis. Biochem Med Metab Biol. 1992, 48(2): 159-173.
    21. Manca D, Ricard A C, Trottier B, Chevalier G. Studies on lipid peroxidation in rat tissues following administration of low and moderate doses of cadmium chloride. Toxicology. 1991, 67(3): 303-323.
    22. Shiraishi N, Uno H, Walkes M P. Effect of L2ascorbic acid pretreatment on cadmium toxicity in the male Fischer ( F344 /NCr) rat. Toxicology. 1993, 85 (223): 85-100.
    23.杨学斌.镉对维生素D代谢的影响及其毒理学.工业卫生与职业病. 2000, 26(4):250-253.
    24. Scott I C, Wslf C H, Akerman K E, Andersson LC. Effects of Cd2 + and Ca2 upon fluxs and proliferation in concanavalin A2Stimulated lymphocytes. Exp Cell Res. 1985, 156(1): 191-197.
    25.徐培娟,于繁荣,古桂雄,李丽.小婴儿血镉含量于生长发育的研究.中国妇幼健康研究. 2006, 17(5): 355-359.
    26. Nordberg G, J in T, Bernard A, et al. Low bone density and renal dysfunction following environmental cadmium exposure in China. Ambio. 2002, 31: 478– 481.
    27.吴思英,田俊,周天枢等.镉污染区居民疾病死亡谱分析.中国公共卫生. 2003, 19 (1): 29-30.
    28.西条旨子,本多隆文.日本卫生学杂志. 2000, 55(1): 235.
    29.孔杏云,何善元,谭小艳.新生儿血镉浓度的性别差异.湖南医科大学学报. 1999, 24(3): 305-306.
    30. Roeleveld N.国外医学卫生学分册. 1992, 3(1): 7-9.
    31. Fery- N, N essmann- C, Girard- F. Toxicologym. 1993, 79(2): 109-118.
    1.史黎薇.铬化合物对健康影响的研究进展.卫生研究. 2003, 32(4): 410-412.
    2.蒋与刚,刘静,庞伟.铬的安全性与毒理学研究进展.国外医学医学地理分册. 2006, 27(3): 97-99.
    3.李桂影.铬中毒的临床反应和实验研究.国外医学医学地理分册. 2002, 23 (1): 33-35.
    4. Shi Liwei. Studies on the effects of chromium complexes. JOURNAL OF HYGIENE RESEARCH. 2003, 32(4): 410~412.
    5.李丁,姚红岩,王淑华,王侠,安静,吴旭.六价铬与骨髓细胞遗传毒性关系探讨.中国公共卫生. 2002, 18(10): 1271.
    6.王亚东,陈琛.铬及其化合物对雄(男)性生殖毒理学研究进展.河南预防医学杂志. 2004, 15(1): 56-58.
    7. Zhang Guang-sheng, Jin Yin-long. Studies on the Nephrotoxicity of Chromium Compounds. Wei Sheng Yan Jiu. 2006, 35(5): 659-662.
    8.武红叶,曾明.六价铬致癌机制的研究进展.癌变、畸变、突变. 2006, 18(6): 491-493.
    9.蔡定邦,洪嘉铭. 170对新生儿与产妇全血微量元素含量的研究.广东微量元素科学. 1995, 2(10): 55-59.
    10. Wong CS, Duzgoren-Aydin NS, Aydin A, Wong MH. Evidence of excessive releases of metals from primitive e-waste processing in Guiyu, China. Environ Pollut. 2007, 148(1): 62-72.
    11. Wong CS, Duzgoren-Aydin NS, Aydin A, Wong MH. Evidence of excessive releases ofmetals from primitive e-waste processing in Guiyu, China. Environ Pollut. 2007, 149(2): 131-40.
    12.徐能义,张玉兰.幼儿血清9种微量元素的调查分析.包头医学院学报. 2000, 16(4): 269-270.
    13. IARC. IARC monographs on the evaluation of carcinogenic risk to humans: chromium, nickel and welding. Lyon: Intern Agency Res Cancer. 1990, 508.
    14. Gunaratnam M, Grant MH. Cr (VI) inhibits DNA, RNA and protein syntheses in hepatocytes: Involvement of glutathione reductase, reduced glutathione and DT-diaphorase.Toxiclo In Vitro. 2008, 24 [Epub ahead of print].
    15. Goldoni M, Caglieri A, Poli D, Vettori MV, Corradi M, Apostoli P, Mutti A. Determination of hexavalent chromium in exhaled breath condensate and environmental air among chrome plating workers. Anal Chim Acta. 2006, 562(2): 229-235.
    16. Arakawa H. A Comparative study of calf thymus DNA binding to Cr (III) and Cr (VI) ions. J Biol Chem. 2000, 275(14): 10150—10153.
    1. Wetmur JG, Lehnert G, Desnick RJ. Theδ–aminolevulinate dehydratase polymorphism: Higher blood lead levels in lead workers and environmentally exposed children with the 1-2 and 2-2 isozymes. Environ Res. 1991, 56(2): 109-119.
    2.郑玉新,王雅文,宋文佳等.δ–氨基乙酰丙酸脱水酶基因多态性与血铅和锌原卟啉的关系.中华预防医学杂志. 2001, 35(2): 96-97.
    3. Schwartz BS, Lee BK, Stewart W, Ahn KD, Springer K, Kelsey K. Associations of delta-aminolevulinic acid dehydratase genotype with plant, exposure duration, and blood lead and zinc protoporphyrin levels in Korean lead workers. Am J Epidemiol. 1995, 142(7): 738-745.
    4. Wetmur J.G, Kaya A.H. et al. Molecular characterization of the humanδ-aminolevulinate dehydratase 2: allele: implication for molecular screening of individuals for genetic susceptibility to lead poisoning. Am. J. Genet, 1991, 49: 757-763.
    5. Raczek E. Polymorphism of delta-aminolevulinate dehydratase in the upper Silesian population, Poland. Hum Hered. 1994, 44(3): 172-174.
    6.吕京,吕新芳,崔涛,谢广云,武荣国,张晨,贺锡雯.中国维吾尔族和彝族人群δ-氨基乙酰丙酸脱水酶基因多态性与铅遗传易感性的关系.中华劳动卫生职业病杂志. 2002, 20(4): 277-281.
    7.郑玉新,宋文佳,王雅文等. 530例中国汉族人口δ-氨基乙酰丙酸脱水酶基因多态性分析.中华预防医学杂志. 2001, 23(3): 175-178.
    8.叶细标,倪为民,杨水莲等. ALAD基因多态性与血铅水平关系的Meta分析.广东微量元素科学. 2001, 8(9): 22-26.
    9.吴胜虎,沉晓明,颜崇淮等.中国汉族儿童ALAD基因型频率分布特点初探.中国当代儿科杂志. 2000, 2(2): 435-438.
    10. Bergdahl IA, Grubb A, Schütz A, Desnick RJ, Wetmur JG, Sassa S, Skerfving S. Lead binding to delta-aminolevulinic acid dehydratase (ALAD) in human erythrocytes. Pharmacol Toxicol. 1997, 81(4): 153-158.
    11. Lin HJ, Han CY, Lin BK, Hardy S. Slow acetylator mutations in the human polymorphic N-acetyltransferase gene in 786 Asians, blacks, Hispanics, and whites: application to metabolic epidemiology. Am J Hum Genet. 1993, 52(4): 827-834
    1.常秀丽.金属硫蛋白及其在镉接触评价中的应用.国外医学卫生学分册, 2004, 31(1): 32-36.
    2.张艳,杨传平.金属硫蛋白的研究进展.分子植物育种. 2006, 4(3): 73-78.
    3.卢坚,金泰,吴训伟.人外周血淋巴细胞中金属硫蛋白基因表达与其对镉易感性的关系.中国公共卫生. 2000, 16(3): 226-228.
    4.孙勇,赵永成,王继先,范亚光,张亚莉,于民,郭国庆,王耐芬,赵金辉.环境镉暴露时胎盘组织金属硫蛋白表达及其意义.中国自然医学杂志. 2005, 7(3): 185-189.
    5.刘志勇,魏国林.金属硫蛋白研究进展.江西科学. 2004, 22(2): 104-109.
    6. Hildebrand CE, Cram LS. Distribution of cadmium in human blood cultured in low levels of CdCl2: accumulation of Cd in lymphocytes and preferential binding to metallothionein. Proc Soc Exp Biol Med. 1979, 161 (4): 438-443.
    7. Yamada H, Koizumi S. Lymphocyte metallothionein-mRNA as a sensitive biomarker of cadmium exposure. Industral Health. 2001, 39(1): 29-32.
    8. Lu J, Jin T, Nordberg G, Nordberg M. Metallothionein gene expression in peripheral lymphocytes from cadmium exposed workers. Cell Stress Chaperones. 2001, 6(2): 97-104.
    9. Bylander JE, Li SL, Sens MA, Sens DA. Exposure of human proximal tubule cells to cytotoxic levels of CdCl2 induces the additional expression of metallothionein 1A Mrna. Toxicol Lett. 1995, 76(30): 209-217.
    10. Yurkow EJ, Makhijani PR. Flow cytometric determination of metallothionein levels in human peripheral blood lymphocytes: utility in environmental exposure assessment. J Toxicol Environ Health. 1998, 54(6): 445-457.
    11. Shaikh ZA, Ellis KJ, Subramanian KS, Greenberg A. Biological monitoring for occupational cadmium exposure: the urinary metallothionein. Toxicol. 1990, 63 (1): 53-62.
    12. Tang W, Kido T, Gross WA, Nogawa K, Sabbioni E, Shaikh ZA. Measurement ofcadmium-induced metallothionein in urine by ELISA and prevention of overestimation due to polymerization. J Anal Toxicol. 1999, 23(3): 153-158.
    13. Hochi Y, Kido T, Nogawa K, Kito H, Shaikh ZA. Dose-response relationship between total cadmium intake and prevalence of renal dysfunction using general linear models. J Appl Toxicol. 1995. 15(2): 109-116.
    14. Kido T, Shaikh ZH, Kito H, Honda R, Nogawa K. Dose-response relationship between urinary cadmium and metallothionein in a Japanese population environmentally exposed to cadmium. Toxicol. 1991, 65(3): 325-332.
    15. Bate LJ, Mulley JC. A BamHI RFLP at MT2A on human chromosome 16. Nucleic Acids Res. 1988, 16(18): 9071.
    16. Hyland VJ, Grist S, West A, Richards RI, Sutherland GR. A 5' flanking region of the metallothionein, MT2A, gene identifies two moderately frequent RFLPs. Nucleic Acids Res. 1987, 15(3): 1350.
    1. Rosen J F. Health Effect of Lead at Low Exposure Levels. Am J Dis Child. 1992, 146:1278.
    2. Iarushkin-Viu. Heavy Metals in the Mother-Newborn Infant Biological System in theTechnology-related Biogeochemical Environment. Gig-Sanit. 1992, 5(6): 13-15.
    3. Schwartz J, Otto D. Lead and Minor Hearing Impair-ment. Arch Environ Health. 1991, 46(5): 300-305.
    4. Marecek J, Shapiro IM, Burke A, Katz SH, Hediger ML. Low-level lead exposure in childhood influences neuropsychological performance. Arch Environ Health. 1983, 38: 355.
    5.张敬旭,符绍莲,胡江等.脐血铅含量与新生儿神经行为发育的关系.中华预防医学杂志. 1997, 31(4): 215-217.
    6.叶萍,尹平,白建桥,刘筱娴,李彦树.影响新生儿神经行为发育的多因素分析.环境与健康杂志. 2003, 20(1): 32-34.
    7.叶萍.铅对儿童神经行为的影响.医学与社会. 2001, 14 (3): 17-19.
    8. Schwartz J, Otto D. Lead and Minor Hearing Impairment. J Arch Environ Health. 1991, 46: 300.
    9. Marecek J, Shapiro IM, Katz SH, et al. Low-level Lead Exposure in Childhood Influence Neuropathological Performance J. Arch Environ Health. 1983, 38: 355.
    10. Yoram Finkelsein.Mechanisms of Lead Neuroloxiciology A.上海国际儿童铅中毒防治研讨会C.中国,上海: 1998.
    11.陶勇.胎儿铅暴露的评价及研究进展.国外医学卫生学分册. 2000, 27(6): 353-355.
    12.刘伟成,李明云.镉毒性毒理学研究进展.广东微量元素科学. 2005, 12(12): 1-4.
    13.刘利娟,丁雄,唐玲等.锌、镉与儿童中枢神经系统疾病51例分析. 1994, 11(4): 59.
    14.马军,欺欣,叶广俊.镉对神经细胞内游离钙的浓度的影响. 1996, 15(1): 21-23.
    15.金念祖,王心如.铬化合物的毒性及其生物学检测指标研究进展. 1999, 25(6): 382-384.
    1.薄梅花,叶葶葶.镉的危害作用与生物检测.劳动医学. 1999, 16(1): 44-46.
    2.刘翔.铬化合物的DNA损伤作用及其机制.癌变、畸变、突变. 1999, 11(1): 60-62.
    3.张波,刘承芸,孟紫强.单细胞凝胶电泳技术在环境污染物检测中的应用.环境科学与技术. 2003, 26(4): 42-44.
    4.周建华,薛莲,时夕金,彭柳明,卞琛.醋酸铅致大鼠血淋巴细胞DNA损伤的研究.中华劳动卫生职业病杂志. 2006, 24(5): 290-292.
    5.懂杰影,金龙金,楼哲丰,郑重,赵惠玲.运用彗星试验检测醋酸铅对小鼠离体、在体生殖细胞的DNA损伤作用.癌变、畸变、突变. 2006, 18(1): 42-45.
    6.伍爱荣,李玉白.四乙基铅对小鼠脑细胞DNA的损伤作用.医学理论与实践. 2006, 19(2): 127-128.
    7.懂淑英,应长青,闻颖,卢明俊.醋酸铅对小鼠免疫细胞增殖和DNA损伤的研究.中华劳动卫生职业病杂志. 2005, 23(6): 457-458.
    8. Xu J ,Lian LJ, Wu C, Wang XF, Fu WY, Xu LH. Lead induces oxidative stress, DNA damage and alteration of p53, Bax and Bcl-2 expressions in mice. Food Chem Toxicol. 2007 Dec 23 [Epub ahead of print].
    9. Gargioni R, Filipak Neto F, Buchi DF, Randi MA, Franco CR, Paludo KS, Pelletier E, Ferraro MV, Cestari MM, Bussolaro D, Oliveira Ribeiro CA. Cell death and DNA damage in peritoneal macrophages of mice (Mus musculus) exposed to inorganic lead. Cell Biol Int. 2006, 30(7): 615-23.
    10. Badisa VL, Latinwo LM, Odewumi CO, Ikediobi CO, Badisa RB, Ayuk-Takem LT, Nwoga J, West J. Mechanism of DNA damage by cadmium and interplay of antioxidant enzymes and agents. Environ Toxicol. 2007, 22 (2): 144-51.
    11. Amara S, Abdelmelek H, Garrel C, Guiraud P, Douki T, Ravanat JL, Favier A, Sakly M, Ben Rhouma K. Influence of static magnetic field on cadmium toxicity: study of oxidative stress and DNA damage in rat tissues. J Trace Elem Med Biol. 2006, 20(4): 263-9.
    12. Toppi L S, Gabbrielli R. Response to cadmium in higher plants. Environ and Exp Botany. 1999, 41: 105-130.
    13. Meng Z Q. Study on Harmful Effect of CdCl2 on Human Blood Lymph Cell by SCG. Guangdong Trace Elements Science. 1998, 5(6): 4-8.
    14. Pennec G L, Pennec M L. Evaluation of the toxicity of chemical compounds using digestive acini of the bivalve mollusc Pecten maximus L. maintained alive in vitro. Aquat Toxicol. 2001, 53: 1-7.
    15. Yu RA, He LF, Chen XM. Effects of cadmium on hepatocellular DNA damage, proto-oncogene expression and apoptosis in rats. Biomed Environ Sci. 2007, 20(2): 146-53.
    16. Jin LJ, Fang ZX, Zhang C, Lou ZF, Dong JY, Chen XW. DNA damage, Bcl-2, Bax expression and ultrastructure change in spermatogenic cell of mice exposed to cadmium. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2005, 23(4): 271-3.
    17. Filipic M, Hei TK. Mutagenicity of cadmium in mammalian cells: implication of oxidative DNA damage. Mutat Res. 2004, 546(1-2): 81-91.
    18. Standeven AM, Wetterhahn KE. Chromium (Ⅵ) toxicity: uptake, reduction, and DNA damage. J A mer Coll Toxicol. 1989, 8: 1275.
    19. Sugiyama M, Tsuzuki K, Hidaka T, et al. Reduction of chromium (Ⅵ) in Chinese hamster Ⅴ- 79 cells. Biol Trace Elem Res. 1991, 30(1): 1.
    20. Vasant C, Balamurugan K, Rajaram R, Ramasami T. Apoptosis of lymphocytes in the presence of Cr (V) complexes: role in Cr (VI)-induced toxicity. Biochem Biophys Res Commun. 2001, 285(5): 1354-60.
    21. Bagchi D, Bagchi M, Stohs SJ. Chromium (VI)-induced oxidative stress, apoptotic cell death and modulation of p53 tumor suppressor gene. Mol Cell Biochem. 2001, 222(1-2): 149-58.
    [1] Morf LS,Tremp J,Gloor R,et al. Brominated flame retardants in waste electrical and electronic equipment: substance flows in a recycling plant [J]. Environ Sci Technol2005, 39: 8691-8699.
    [2]杨子江.电子垃圾的资源化研究[J].节能与环保,2003,10(6): 16-18.
    [3]张敦信,吕锋,彭秀丽.废旧电脑的环境污染与防治[J].城市管理与科技,2004,6 (1): 28-30.
    [4] Hamers T,Kamstra JH,Sonneveld E,et al. In vitro profiling of the endocrine-disrupting potency of brominated flame retardants [J]. Toxicol Sci, 2006, 92: 157-173.
    [5] Reistad T,Mariussen E,Fonnum F. The effects of brominated flame retardants on cell death and free radical formation in cerebellar granule cells [J]. Organohalog Compd, 2002, 57: 391-394.
    [6] Kodavanti PR,Derr-Yellin E.Differential effects of polybrominated diphenyl ethers and polychlorinated biphenyls on [3H]arachidonic acid release in rat cerebellar granule cells[J]. Toxicol Sci, 2002, 68: 451-457.
    [7] Brouwer A,Morse DC,Lans MC,et al. Interaction of persistent environmental organohalogns with the thyroid hormone system: mechanisms and possible consequences for animal and human health [J]. Toxicol Ind Health, 1998, 14(1~2): 59-84.
    [8] Fowles JR,Fairbrother A,Baecher-Steppan L,et al.Immunologic and endocrine effects of the flame-retardant pentabromodiphenyl ether(DE-71) in C57BL/6J mice [J]. Toxicology, 1994, 86: 49-61.
    [9] Zhou T,TaylorMM,de Vito MJ,et al. Developmental exposure to brominated diphenyl ethers results in thyroid hormone disruption [J]. Toxicol Sci, 2002, 66: 105-116.
    [10] International Program on Chemical Safety.Environmental Health Criteria Brominated diphenyl ethers [R]. Geneva: WHO, 994, No.162.
    [11] Legler J, Brouwer A. Are brominated flame retardants endocrine disruptors? Environ Int. 2003, 29(6): 879~885.
    [12] Hardy ML.The toxicology of the three commercial polybrominated diphenyl oxide (ether) flame retardants. Chemosphere. 2002, 46(5): 757~777.
    [13] National Toxicology Program. NTP Toxicology and Carcinogenesis Studies of Polybrominated Biphenyls (CAS No.67774-32-7) (Firemaster FF-1(R)) in F344/N Rats and B6C3F1 Mice (Feed Studies). Natl Toxicol Program Tech Rep Ser. 1993, 398: 1~235.
    [14] Meerts IATM, Assink Y, Cenjin PH, et al. Distribution of the flame retardant tetrabromobisphenol A in pregnant and fetal rats and effect on thyroid hormone homeostasis. Organohalog Compd. 1999, 40: 375~378.
    [15] IPC (International Program on Chemical Safety).Environmental Health Criteria no.172.Tetrabromobisphenol A and derivates. WHO, Geneva, 1995.
    [16] Meerts IATM, Van Zanden JJ, Luijks EAC, et al. Potent competitive interactions of some brominated flame retardants and related compounds with human transthyretin in vitro. Toxicol Sci. 2000, 56: 95~104。
    [17] Canesi L, Lorusso LC, Ciacci C,et al. Effects of the brominated flame retardant tetrabromobisphenol-A (TBBPA) on cell signaling and function of Mytilus hemocytes: involvement of MAP kinases and protein kinase C [J]. Aquat Toxicol, 2005, 75: 277-287.
    [18] Tada Y,Fujitani T,Yano N,et al. Effects of tetrabromobisphenol A,brominated flame retardant,in ICR mice after prenatal and postnatal exposure [J]. Food Chem Toxicol, 2006, 44: 1408-1413.
    [19] Frydrych B,Szymanska JA. Nephrotoxicity of tetrabromobisphenol A in rats after repeated exposure [J]. Bromatol Chem Toksykol, 2001, 34: 1-5.
    [20] Meerts IATM , Assink Y , Cenjin PH , et al. Distribution of the flame retardant tetrabromobisphenol A in pregnant and fetal rats and effect on thyroid hormone homeostasis [J]. Organohalog Compd, 1999, 40: 375-378.
    [21] Dean WP, Jessup DC, Epstein WL, et al.Tetrabromobisphenol A Modified Draize multiple insult test in humans. Mattawan, Michigan, International Research and Development Corporation (report to Velsicol Chemical Corp., submitted to WHO by the Brominated Flame Retardant Industry Panel), cited in IPCS, 1995.
    [22] National Chemicals Inspectorate. Risk assessment-hexabromocyclododecane (CAS-No.25637-99-4;EINECS-No.247-148-4)[R]. Sweden, 2002: 9.
    [23] Chngelis CP.A 28-day repeated dose oral toxicity study of HBCD in rats[R]. Ashland,OH,USA:WiL Research Laboratories, USA, 1997: 925.
    [24] Chengelis CP.A90-day oral (gavage) toxicity study of HBCD in rats[R].Ashland, OH, USA: Wil Research Laboratories, USA, 2001: 1527.
    [25] Zeller H, Kirsch P.Hexabromocyclododecane: 28-day feeding trials with rats. Cited in KEMI. 2002.
    [26] Darnerud PO. Toxic effects of brominated flame retardants in man and in wildlife. Environ Int. 2003, 29(6): 841~853.
    [27] National Chemicals Inspectorate. Risk assessment-hexabromocyclododecane (CAS-No.25637-99-4;EINECS-No.247-148-4)[R]. Sweden,2002:9.
    [28] National Toxicology Programme. Toxicology and carcinogenesis studies of polybrominatd biophnyls (Firemaster FF-1) (CAS No. 67774-32-7) in F344/…6777-32-7) IN F344/N RATS AND B6C3F1 MICE (feed studies) [R].NTPTR39, NIH publication, 1993:2892-2853.
    [29] ATOCHEM. Decabromobiphenyl. Paris La Defe`NSE, France, 1990.

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