铅暴露对6～12岁儿童健康状况影响

目的 探讨南方某地6～12岁儿童铅暴露对健康损害状况.方法 采用分层随机抽样方法,选择某地6～12岁儿童进行问卷调查、健康体检、智力测试、Conners行为测试;采集儿童血、尿样,检测血铅浓度,全血锌原卟啉(ZPP)、尿δ氨基-γ-酮戊酸(AIA)含量及血δ-氨基-γ-酮戊酸脱氢酶(ALAD)活性.结果 309名儿童血铅浓度几何均值为71.2μg/L,zPP 0.15μg/g Hb,ALA 24.4μg/L,ALAD活性328.9 U.54(17.5%)名儿童血铅≥100μg/L.血铅<100μg/L儿童zPP与血铅呈负相关(r=-0.240),≥100 μg/L儿童zPP与血铅呈正相关(r=0.403).ALAD与血铅呈负相关(r=-0.287).血铅≥100μg/L儿童存在一定行为改变,身高、免疫力及智力水平低于血铅<100 μg/L儿童.结论 该地儿童的铅暴露使体内相关酶含量、活性改变,且与儿童身高发育、免疫力、智力水平下降及行为改变有关.     

δ-氨基-γ-酮戊酸脱水酶基因多态性与维吾尔族、汉族儿童铅中毒遗传易感性

目的探讨维吾尔族和汉族儿童δ-氨基-γ-酮戊酸脱水酶(ALAD)基因多态性及其与铅中毒遗传易感性的关系。方法PCR-RFLP方法对新疆乌鲁木齐市的维吾尔族443名和汉族469名儿童ALAD基因多态性进行分析。应用单因素和多因素分析探讨了维吾尔族和汉族儿童ALAD基因多态性与血铅水平的关系,及影响血铅水平的因素。结果在维吾尔族人群中,ALAD1和ALAD2等位基因频率分别为90.52%和9.48%;在汉族人群中,ALAD1和ALAD2等位基因频率分别为95.73%和4.27%;两者差异有统计学意义(P<0.01)。维族儿童血铅浓度为(55.86±2.23)μg/L,铅中毒流行率为23.25%;汉族儿童血铅浓度为(53.05±2.24)μg/L,铅中毒的流行率为23.31%,两民族血铅水平和铅中毒流行率之间均无统计学意义(P>0.05)。结论维吾尔族和汉族儿童ALAD基因多态性与血铅水平间无相关关系。     

ALAD基因多态性与儿童血铅水平关系研究

目的探讨影响儿童血铅水平的因素,以及血铅水平与ALAD基因多态性之间的关系。方法对2016年云南省某铅冶炼厂周边某小学1~3年级281名学生进行研究。用调查表对调查对象一般情况进行收集;测量身高、体重等发育指标;同时采集外周静脉血样,进行ALAD基因分型以及血铅检测。结果 ALAD1-2组儿童血铅水平[(114.71±96.11)mg/L]高于ALAD1-1组[(87.17±73.11)mg/L],但差异无统计学意义。不同年龄组间的血铅水平差异有统计学意义(F=8.826;P0.01);进一步对影响血铅水平的因素进行多元回归分析发现,儿童血铅水平与年龄呈负相关(r=-0.197,P0.01)。结论较低血铅水平儿童ALAD基因多态性与血铅水平的关系需进一步进行研究。儿童的血铅水平与年龄呈负相关。儿童血铅水平由遗传因素和环境因素共同决定,加强对儿童良好生活习惯的健康教育,必要时可同时进行行为学的干预,可有效地降低儿童的血铅水平。     

基质γ-羧基谷氨酸蛋白和氨基乙酰丙酸脱水酶基因多态性与儿童血铅的关系

[目的]探讨基质γ-羧基谷氨酸蛋白(MGP)和氨基乙酰丙酸脱水酶(ALAD)基因多态性在儿童铅中毒发生过程中的作用。[方法]测定了345名6-12岁的中国汉族儿童的血铅水平;采用多聚酶链反应-限制性片段长度多态性法(PCR-RFLP)分析MGP和ALAD基因的多态性。[结果]在ALAD基因未发生变异的情况下,MGP基因变异导致血铅水平降低;携带ALAD1-2、ALAD2-2或MGP TT基因型儿童的血铅水平(2．32μmol/L)高于携带ALAD1-1和MGP CT、MGP CC基因型儿童(2．18μmol/L),差异有统计学意义(P=0．0091)。[结论]MGP和ALAD基因多态性可影响儿童铅中毒的易感性,ALAD1-2、ALAD2-2或MGP TT基因型可能是儿童铅中毒的易感基因型。     

鞍山市学龄前儿童血铅及脂质过氧化水平检测

目的 探讨环境铅暴露对学龄前儿童血铅及脂质过氧化水平的影响.方法 采用分层整群抽样法,抽取辽宁省鞍山市5所托幼机构的408名学龄前儿童,其中男童217名,女童192名.检测血铅、全血δ-氨基γ-戊二酸脱水酶(ALAD)、超氧化物歧化酶(SOD)、还原型谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GSH-Px)和血清丙二醛(MDA).结果 鞍山市儿童铅中毒发生率为27.4%;血铅≥100 μg/L的儿童ALAD活性为(644.50±146.17)u/(g·Hb),与血铅<100μg/L的儿童比较明显降低,MDA水平达(5.875±0.818)nmol/ml,与血铅<100μg/L的儿童比较明显升高;被调查儿童的SOD、GSH-Px、GSH水平与血铅升高无关联.结论 ALAD和MDA是反映铅致氧化损伤的敏感指标.     

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

目的　探讨δ 氨基乙酰丙酸脱水酶 (ALAD)基因多态性与血铅和锌原卟啉之间的关系。方法　采样分析 370名严重铅污染区儿童的血铅、锌原卟啉和ALAD基因型。结果　ALAD1 2 / 2 2 基因型的血铅水平 (2 6 2 1± 0 5 6 1) μmol/L高于ALAD1 1基因型 (2 36 0± 0 5 96 ) μmol/L ;而锌原卟啉水平也增高 ,前者 (13 0 7± 9 38) μmol/L ,后者 (9 90± 6 30 ) μmol/L。 结论　在同样的高铅暴露条件下 ,ALAD1 2 / 2 2 基因型可影响儿童体内铅负荷水平以及铅所致血液毒性效应     

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

目的　探讨我国维吾尔族、彝族人群δ 氨基乙酰丙酸脱水酶 (ALAD)基因多态性与铅遗传易感性的关系。方法　采用多聚酶链式反应 (PCR)和限制性内切酶 (MspI)限制性片断长度多态性(RFLP)方法分析 2 14名新疆维吾尔族人和 14 4名云南彝族人的ALAD基因多态性及等位基因分布 ;运用单因素和多因素分析探讨了维吾尔族和彝族人群ALAD基因多态性与血铅水平的相关关系 ,及影响血铅水平的因素。结果　维族人群ALAD1和ALAD2 等位基因分布频率分别是 0 .91和 0 .0 9;彝族人群ALAD1和ALAD2 等位基因频率分别是 0 .98和 0 .0 2。维族人群的血铅均值为 (76± 4 ) μg/L ,血铅≥10 0 μg/L的比例为 2 5 .7% ;彝族人群的血铅均值为 (5 0± 16 ) μg/L ,血铅≥ 10 0 μg/L的比例为 6 .3%。未见本研究人群ALAD等位基因的多态性与血铅水平有相关关系。结论　ALAD基因多态性对铅毒性影响的方式可能与机体铅的负荷量密切相关     

重组人生长激素对生长激素缺乏症儿童生长及骨代谢的影响

目的研究生长激素缺乏症(GHD)儿童用生长激素治疗前后的身高、骨龄、骨代谢指标的改变。方法测定48例生长激素缺乏症(GHD)儿童的身高、骨龄、身高增长速率、血清骨代谢指标[骨碱性磷酸酶(BAP)、骨钙素(Osteocalcin)、类胰岛素生长因子1(Insulin like growth factor 1,IGF-1)、胰岛素样生长因子结合蛋白3(Insulin-like growth factor binding protein-3,IGFBP-3)、1,25-(OH)_2D_3],比较各组差异。结果 r-h GH治疗后6、12个月时GHD儿童身高增长速度较治疗前明显加快,血清BAP、Osteocalcin、IGF-1、IGFBP-3、1,25-(OH)_2D_3水平较治疗前明显增高。结论 GHD儿童体内骨代谢水平明显降低,GH替代治疗6个月和12个月后,IGF-1、IGFBP-3、身高、骨代谢指标、骨代谢调节激素1,25-(OH)_2D_3明显增高,GH替代治疗可促进GHD儿童身高增长及骨代谢。     

矮小症儿童血清内IGF-1、IGFBP-3检测的意义

目的探讨矮小症儿童血清内胰岛素样生长因子-l(IGF-l)和胰岛素样生长因子结合蛋白-3(IGFBP-3)浓度变化情况,寻找一种简便确诊生长激素缺乏症的方法。方法对82例矮小症患儿选用精氨酸和左旋多巴激发试验检测血清中生长激素(GH)水平,设定两项药物激发试验GH峰值均l0ug/L即诊断为生长激素缺乏(GHD组,50例),有一项激发试验GH峰值l0ug/L诊断为特发性矮小症(ISS组,32例),选取40例健康儿童作为对照组,用电化学发光法检测血清IGF-l和IGFBP-3水平。结果 IGF-1、IGFBP-3检测结果 GHD组与ISS组比较有统计学差异(P0.05),ISS组与对照组比较有统计学差异(P0.05),GHD组与对照组比较有统计学差异(P0.01)。结论血清IGF-1和IGFBP-3的浓度与GH峰值有很好的正相关性,单次检测血清中IGF-1和IGFBP-3的浓度可以诊断矮小症儿童的生长激素缺乏,不失为一种简便方法,可以临床应用。     

ALAD基因多态性对铅的肾脏毒性易感性作用

目的探讨δ-氨基-γ-酮戊酸脱水酶(ALAD)基因多态性是否对铅肾脏毒性易感性产生影响。方法抽取某钢铁企业的142名男性铅接触炉前工作为研究对象,收集基本信息,采集外周静脉血,检测血铅及相关指标、肾功能指标(血清肌酐、肌酐清除率、血尿素氮、和氨基-乙酰-β-葡萄糖苷酶),同时采用实时定量-聚合酶链反应(RT-PCR)进行ALAD基因型测定,估计累积铅暴露,进行ALAD基因多态性与肾脏损害易感性分析。结果 142名铅接触工人中ALAD1-1基因型有120人(84.51%),ALAD1-2基因型有22人(15.49%),未发现ALAD2-2基因型。等位基因ALAD-1和ALAD-2的频率分别为92.25%和7.75%。ALAD1-2基因型组血铅水平和肌酐清除率分别高于ALAD1-1基因型组的个体,差异有统计学意义(均有P<0.05),ALAD1-2基因型组平均血清肌酐低于ALAD1-1基因型组,差异有统计学意义(P<0.05)。低累积铅暴露时,肌酐清除率随着暴露剂量的增加而升高;但高累积铅暴露时,肌酐清除率随着暴露剂量的增加而下降,而且ALAD1-2基因型个体随着暴露剂量的增加下降更为明显。结论在相同铅暴露情况下,ALAD1-2基因引起血铅升高,进而可能影响血清肌酐和肌酐清除率,而这种作用在累积铅暴露达到一定高的阈值时才显示出来,说明ALAD1-2基因多态性会增加铅慢性肾功能损害的易感性风险。     

锌原卟啉作为环境铅污染人群筛查指标的可行性研究

目的探讨红细胞锌原卟啉（ZPP）应用于人群接触环境铅污染筛查指标的可行性。方法以紫金县某电池厂附近常住居民为调查对象,采集被调查者静脉血2～3 mL,采用血液锌原卟啉测定仪测定ZPP、石墨炉原子吸收光谱法测定血铅。儿童以血铅含量≥100μg/L、成年人以≥400μg/L为慢性铅中毒判定标准。结果共调查946名居民,其中1～13岁儿童174人、16～87岁成年人772人。儿童血铅含量超标率为14.9%（26/174）,儿童ZPP含量中位数为0.780μmol/L,血铅中位数为47.675μg/L,儿童ZPP含量与血铅含量的相关关系没有统计学意义（P〉0.05）。成人血铅含量超标率为9.5%（73/772）,成人ZPP含量中位数为0.740μmol/L,血铅中位数为69.572μg/L,成人ZPP含量与血铅含量呈弱相关关系（r=0.344,P〈0.05）。儿童血铅高水平组（血铅≥100μg/L）ZPP含量与血铅含量呈较强的相关关系（r=0.530,P〈0.05）,儿童血铅低水平组（血铅〈100μg/L）ZPP含量与血铅含量的相关关系没有统计学意义（P〉0.05）。成人血铅高水平组（血铅≥400μg/L）和低水平组（血铅〈400μg/L）的ZPP含量与血铅含量均具有相关关系（r分别为0.566、0.142,均P〈0.05）。结论成人血铅或儿童血铅水平较高时,ZPP可以作为环境铅污染人群筛查的指标。     

Adverse effects in workers exposed to inorganic lead

This paper describes a retrospective cohort study comparing 60 workers occupationally exposed to inorganic lead and 60 matched controls. All subjects were assessed using data obtained from a specially designed Questionnaire for lead exposure and toxic effects assessment, physical examination, spirometry, ECG, and laboratory tests including blood lead level (BLL) and biomarkers of lead toxic effects. Muscle pain, droopiness, and work-related nasal symptoms were significantly more frequent in lead workers. The prevalence of lung symptoms was higher in lead workers than in controls, but not significantly (20 % vs. 6.6 %, respectively). Mean values of BLL and delta-aminolevulinic acid (ALA) were significantly higher in lead workers. The activity of delta-aminolevulinic acid dehydratase (ALAD) in lead workers was significantly lower than in controls. Abnormal of BLL, ALAD, and ALA were more frequent in lead workers, with statistical difference for BLL and ALAD. Inverse correlation was found between BLL and ALAD, and positive correlation between BLL and age, years of employment, and years of exposure. Inverse correlation was found between ALAD and age, years of employment, years of exposure, blood pressure, alcohol consumption, and years of alcohol consumption. Changes in spirometry correlated inversely with BLL. A positive correlation was found between BLL and erythrocyte count and haemoglobin concentration, whereas it was inverse for ALAD and haemoglobin concentration. A significant difference was found for BLL and ALAD, with a very high odds ratio (14.64 and 7.23, respectively) and high relative risk (4.18 and 3.08, respectively). Our data have confirmed the association between occupational lead exposure and deviation in specific biological markers of lead effect and between the role of occupational exposure in the development of adverse effects.     

Blood lead levels and associated sociodemographic factors among preschool children in the South Eastern region of China

Children are especially vulnerable to lead toxicity, and exposure to lead has been linked to poor school performance and delinquency in children and adolescents. Even low-level lead exposure [blood lead level (BLL) <10 μg/dL] can cause intellectual deficit. In China, BLLs in children decreased slightly after the phasing out of lead in gasoline, but few studies have examined the sociodemographic factors associated with BLL above 10 μg/dL. In this study, we sought to examine the hypothesis that sociodemographic factors predict BLLs. We measured BLLs of 1344 preschool children (3-5 years old) from the China Jintan Child Cohort Study. Children's sociodemographic and health statuses, as well as parental sociodemographic data, were collected using questionnaires. Regression models were used to explore the association between sociodemographic factors and log-transformed BLLs as well as the relationship between sociodemographic factors and the risk of BLL ≥10 μg/dL. We found the median BLL to be 6.2 μg/dL (range: 1.8-32.0 μg/dL); 8% of children had BLLs ≥10 μg/dL. Boys had a higher median BLL (6.4 μg/dL) than girls and were more likely to have BLL ≥10 μg/dL [odds ratio = 1.77, 95% confidence interval 1.14, 2.74]. BLLs increased as children aged, with a median BLL of 6.6 μg/dL among 5-year-old children. Children with siblings had a higher average BLL and greater prevalence of a BLL ≥10 μg/dL than those without siblings. Living in a crowded neighbourhood was also associated with increased BLLs. Mother's lower education, father's occupation (as professional worker) and parental smoking at home were associated with increased BLLs. This study shows that children in this area still have relatively high BLLs even after the phasing out of leaded gasoline. Both children's and parental factors and community condition are associated with increased BLLs. Future efforts are needed to identify other sources of exposure and develop targeted prevention strategies.     

Determinants of blood lead levels in children: a cross-sectional study in the Canary Islands (Spain)

The adverse effects of lead exposure on children are well known. Low blood lead levels (BLL) produce neurodevelopmental delay and cognitive disorders. However, since BLL thresholds for adverse effects on children's health are not known, the children population at risk of excessive lead exposure still has to be identified. This study was aimed at evaluating BLL in a children population of Gran Canaria (Canary Islands, Spain). Up to our knowledge, this is the first study to report on BLL in this population. Lead was identified and quantified in blood samples of 120 children, by means of Graphite furnace atomic absorption spectrometry (GFAAS). Lead was undetected in 80% of samples; BLL was 1 to 5 μg/dl in 15% of samples, and higher than 5 μg/dl in more than 4% of samples. BLL values in the evaluated children were low and similar to those described for other populations in Western countries. However, samples with the highest contamination (those in percentile 95) reached BLLs as high as 5.2 μg/dl. Positive associations were found between BLL and recent immigration (children adopted from non-western countries), and between BLL and parental smoking in children with low weight at birth. Since lead exposure in childhood may be a causative factor in adverse health trends - especially those involving the neurological system - and since threshold values for adverse lead effects are unknown, our finding that around 20% of the studied children had BLL higher than 1 μg/dl are of concern. Enhancing preventive measures for reducing lead exposure in children from the Canary Islands deserves further study.     

Lead and delta-aminolevulinic acid dehydratase polymorphism: where does it lead? A meta-analysis

BACKGROUND: Lead poisoning affects many organs in the body. Lead inhibits delta-aminolevulinic acid dehydratase (ALAD), an enzyme with two co-dominantly expressed alleles, ALAD1 and ALAD2. OBJECTIVE: Our meta-analysis studied the effects of the ALAD polymorphism on a) blood and bone lead levels and b) indicators of target organ toxicity. DATA SOURCE: We included studies reporting one or more of the following by individuals with genotypes ALAD1-1 and ALAD1-2/2-2: blood lead level (BLL), tibia or trabecular lead level, zinc protoporphyrin (ZPP), hemoglobin, serum creatinine, blood urea nitrogen (BUN), dimercaptosuccinic acid-chelatable lead, or blood pressure. DATA EXTRACTION: Sample sizes, means, and standard deviations were extracted for the genotype groups. DATA SYNTHESIS: There was a statistically significant association between ALAD2 carriers and higher BLL in lead-exposed workers (weighted mean differences of 1.93 microg/dL). There was no association with ALAD carrier status among environmentally exposed adults with BLLs < 10 microg/dL. ALAD2 carriers were potentially protected against adverse hemapoietic effects (ZPP and hemoglobin levels), perhaps because of decreased lead bioavailability to heme pathway enzymes. CONCLUSION: Carriers of the ALAD2 allele had higher BLLs than those who were ALAD1 homozygous and higher hemoglobin and lower ZPP, and the latter seems to be inversely related to BLL. Effects on other organs were not well delineated, partly because of the small number of subjects studied and potential modifications caused by other proteins in target tissues or by other polymorphic genes.     

铅作业工人血铅水平和肝功能状况及其影响因素

目的 了解铅作业工人血铅水平及肝功能状况,分析其影响因素,为保护工人健康提供依据。
方法 选择某铅酸蓄电池公司1 179名体检工人为研究对象。接触组为一线接触铅的801名工人,对照组为该企业行政、后勤类等378名非铅接触者。采用问卷调查和健康体检相结合的方法,收集工人基础信息并进行数据分析。
结果 铅作业工人血铅水平范围为89~463 μg/L,其M（P₂₅,P₇₅）为152.2（65.4,356.7）μg/L,血铅超标率（血铅值≥400 μg/L）为10.2%。铅接触组血铅异常率高于对照组,差异有统计学意义（P < 0.01）。logistic回归分析发现接触组血铅升高的风险是对照组的7.321倍（P < 0.01）;血铅水平> 200~300 μg/L组、> 300~400 μg/L组及> 400 μg/L组发生肝功能异常的风险为 < 100 μg/L组的1.775倍、2.659倍和3.114倍（P均 < 0.05）,10~13年工龄组及5~ < 10年工龄组发生肝功能异常的风险是 < 5年组的1.454倍和1.122倍（P < 0.05）;血铅水平> 200~300 μg/L组、> 300~400 μg/L组及> 400 μg/L组发生肝脏B超异常的风险为 < 100 μg/L组的1.650倍、2.219倍和2.658倍（P均 < 0.05）,铅接触组B超异常风险是对照组的2.235倍（P < 0.05）。
结论 职业铅接触引起工人血铅水平升高,血铅是肝功能和肝脏B超异常的独立危险因素,故应加强工人健康监护。
     

Modification by ALAD of the Association between Blood Lead and Blood Pressure in the U.S. Population: Results from the Third National Health and Nutrition Examination Survey

Background

Environmental lead exposure has been found to be associated with an increased risk of hypertension. Individuals vary greatly in susceptibility to lead toxicity, and genetic susceptibility has often been cited as the probable cause for such variation.

Objective

The main objective is to determine the role of the aminolevulinic acid dehydratase (ALAD) gene, which encodes the main carrier protein of lead in blood, in the association between lead exposure and blood pressure (BP) and hypertension in the U.S. population.

Methods

We analyzed data from individuals ≥ 17 years of age who participated in the Third National Health and Nutrition Examination Survey for whom DNA was available (n = 6,016). Multivariable logistic and linear regressions stratified by race/ethnicity were used to examine whether hypertension and BP were associated with ALAD and blood lead levels (BLL).

Results

BLL was associated with systolic BP in non-Hispanic whites and with hypertension and systolic and diastolic BP in non-Hispanic blacks. BLL was not associated with BP outcomes in Mexican Americans. Non-Hispanic white ALAD2 carriers in the highest BLL quartile (3.8–52.9 μg/dL) had a significantly higher adjusted prevalence odds ratio for hypertension compared with ALAD1 homozygous individuals. We also found a significant interaction between lead concentration and the ALAD2 allele in non-Hispanic whites and non-Hispanic blacks in relation to systolic BP.

Conclusions

BLL may be an important risk factor for hypertension and increased systolic and diastolic BP. These associations may be modified by ALAD genotype.     

维生素D受体基因(VDR)多态性与儿童铅中毒易感性的研究

目的:观察维生素D受体(VDR)基因rs731236、rs1544410及rs7975232在深圳市儿童血铅≥60μg/L样本组和低铅对照组之间的分布,揭示VDR基因多态性与儿童铅中毒易感的相关性。方法:在6个月～6岁儿童中筛选出75例样本组(血铅≥60μg/L均值(X=82.24μg/L)和80例对照组(血铅均值X=19.90μg/L)的样本,用PCR方法对VDR基因rs731236、rs1544410及rs7975232进行扩增,采用基质辅助激光解吸电离飞行时间质谱分析法(MALDI-TOF-MS)鉴定其基因型,比较各基因型在两组间的分布,寻找其与儿童血铅值的关系。结果:VDR基因rs731236中的基因型TT在样本组与对照组的分布频率差异有统计学意义(P<0.05),rs1544410中的GG在样本组与对照组的分布频率差异有统计学意义(P<0.01),rs7975232多态性在样本组与对照组的分布频率差异无统计学意义(P>0.05)。结论:VDR基因rs731236中的TT和rs1544410中的GG基因型可能增加儿童铅中毒的危险性;作为铅中毒的易感基因筛查值得进一步探讨。     

Delta-aminolevulinate dehydratase polymorphism and blood lead levels in Chinese children

This study investigated the relationship between the delta-aminolevulinate dehydratase (ALAD) isozymes and the blood lead levels of Chinese children. The purpose of this study was to determine the precise ALAD genotyping in Chinese children and identify the contribution of the ALAD genotype to the body lead burden. Blood samples were obtained from 109 boys and 120 girls. These children were 6-10 years old and from a single primary school. Both the school and their homes were within a community in which a large smelter was located. An environmental questionnaire was obtained for each subject, and blood lead levels and ALAD isozyme phenotype were analyzed in a double-blinded fashion. The blood lead levels of 229 children ranged from 4.5 to 26.4 microg/dl; the mean was 10.3 microg/dl and the standard deviation was 3.3 microg/dl. The gene distribution of the ALAD isozyme phenotypes in these environmentally exposed children was ALAD 1-1 (92%), ALAD 1-2, (8%), and ALAD 2-2 (0%). The mean blood level of the environmentally exposed children, who were homozygous for the ALAD1 allele, was 9.7 microg/dl; the mean for those who were heterozygous for the ALAD2 allele was 11.7 microg/dl. Using the t test, the means of the groups were different at the level of t=2.2058, P<0.05. Step-wise regression and multiple analyses of covariance were employed to control the confounders to measuring the independent contribution of the ALAD genotype on blood lead levels. After controlling the confounders, the contribution of the ALAD genotype to the blood lead level was greater and still statistically significant (F=7.3201, P<0.01). These results indicate that individuals carrying the ALAD2 allele are more likely to have sustained increases in blood lead levels when exposed to a lead-contaminated environment.