砷染毒大鼠生精细胞凋亡及端粒酶活力的变化

目的观察不同剂量的染砷(As2O3)大鼠生精细胞凋亡及端粒酶活力表达的变化。方法将40只健康雄性清洁级SD大鼠随机分成4组,分别为低、中、高剂量(0.375、0.75、1.5 mg/kg)砷染毒组和对照组,以灌胃法连续染毒16周后计算各组大鼠精子头计数,并计算睾丸脏器系数、每日精子生成量(DSP)。采用TUNEL原位细胞杂交方法检测大鼠生精细胞凋亡,免疫组化法检测大鼠生精细胞端粒酶活力的表达。结果与对照组比较,中剂量组(0.75 mg/kg)和高剂量组(1.5 mg/kg)睾丸精子头计数和DSP均显著降低(P<0.01),生精细胞凋亡指数(AI)显著升高(P<0.01),生精细胞端粒酶活力表达明显降低(P<0.01);每日精子生成量与生精细胞凋亡呈负相关(r=-0.563,P<0.01);生精细胞凋亡与端粒酶活力呈负相关(r=-0.896,P<0.01)。结论一定剂量的As2O3可通过抑制生精细胞端粒酶活力,促进生精细胞凋亡而导致精子生成量减少,产生雄性生殖毒性。     

亚慢性砷暴露对大鼠海马组织BDNF表达的影响

目的探讨亚慢性饮水型砷暴露对大鼠海马组织BDNF表达的影响。方法将40只SD大鼠按体重随机分为4组,分别为对照组(蒸馏水)和2.4、12、60 mg/L亚砷酸钠溶液染毒组,每组10只,雌雄各半,采用自由饮水的方式连续染毒100 d。检测脑砷含量、海马组织BDNF mRNA及蛋白表达。结果各染砷组大鼠脑砷含量均高于对照组(P0.05),且脑砷含量随着染毒剂量的增加呈上升趋势;各染砷组大鼠海马组织BDNF mRNA及其蛋白表达均低于对照组(P0.05)。结论亚慢性砷暴露可引起大鼠海马组织BDNF mRNA及其蛋白表达的降低。     

慢性砷中毒对大鼠肾近曲小管上皮细胞凋亡表达的影响

目的探讨慢性砷中毒对大鼠近曲小管上皮细胞凋亡表达的影响。方法将30只健康成年清洁级SD大鼠随机分为高(10.0mg/kg)、低(0.4mg/kg)剂量砷染毒组和对照(蒸馏水)组,采用经口自由饮用方式进行染毒,日饮水量约为200ml/kg,连续染毒6个月。染毒结束后,取大鼠肾脏进行HE染色和PAS染色,采用免疫组化法(TUNEL细胞凋亡染色法)测定大鼠近曲小管上皮凋亡细胞计数及其灰度值。结果砷中毒大鼠近曲小管上皮细胞空泡样变性,细胞腔面刷状缘减少并脱落,可见细胞核固缩、深染,有较多凋亡细胞,染色质浓缩聚集于核膜下。与对照组比较,高、低剂量砷染毒组大鼠肾近曲小管上皮凋亡细胞计数增高,灰度值较低,差异均有统计学意义(P0.05)。随着砷染毒剂量的增高,大鼠肾近曲小管上皮凋亡细胞计数呈增多趋势,灰度值呈降低趋势。结论慢性砷中毒可引起大鼠近曲小管上皮细胞凋亡。     

亚慢性砷染毒对大鼠肾小球细胞半胱氨酸蛋白酶-3表达的影响

目的探讨半胱氨酸蛋白酶-3(caspase-3)对砷中毒肾小球细胞凋亡的影响。方法将清洁级SD大鼠随机分为高、低剂量组和对照组(自来水),每组10只,雌雄各半,将As2O3溶于饮水中进行染毒。高、低剂量组砷染毒剂量分别为10、0.4mg/(kg·d),对照组可自由饮水,连续染毒4个月,每周称体重。染毒结束后,测定尿砷、血砷的含量,免疫组化SABC方法检测肾小球细胞caspase-3的表达,并进行图像分析、计数。结果与对照组比较,高、低剂量组尿砷、血砷含量均较高,肾小球细胞caspase-3阳性细胞数均较多,灰度值均较低;与低剂量组比较,高剂量组尿砷、血砷含量均较高,肾小球细胞caspase-3阳性细胞数较多,灰度值较低,差异均有统计学意义(P<0.01)。结论慢性砷中毒所致肾小球细胞凋亡可能与肾小球细胞caspase-3的表达明显增加有关。     

砷诱发细胞凋亡与大鼠畸胎形成的关系研究

为进一步揭示砷的致畸性、胚胎毒性和作用机制，采用胚胎活体染色和原位ＤＮＡ末端标记等技术探讨了不同剂量砷是否能诱导孕９．５天龄大鼠的胚胎细胞发生凋亡（程序性细胞死亡）及其凋亡与畸胎形成的关系。结果表明随着砷浓度（０、１、４和８ｍｇ／ｋｇ）的增高，畸胎率和死胎率分别由２．６％和０上升到３５．７％和２３．８％，呈明显剂量－反应关系。活体染色发现在胚胎脑、眼、体节、肢芽和腮弓等部位出现大量散在的凋亡细胞，与畸形发生部位相一致。原位ＤＮＡ末端标记进一步证实砷能诱发器官形成期胚胎细胞凋亡，８ｍｇ／ｋｇ砷染毒后，凋亡阳性率高达５５．６％（Ｐ＜０．０５），表明凋亡与畸胎发生关系密切，这是砷致畸作用的重要机制之一。实验结果还发现胚胎细胞坏死亦与畸胎形成有关。     

姜黄素对砷致大鼠睾丸生精细胞凋亡的拮抗作用

目的研究姜黄素对砷致大鼠睾丸生殖细胞凋亡的拮抗作用。方法将50只健康清洁级Wistar雄性大鼠随机分为5组,分别为对照(双蒸水)组和亚砷酸钠(100 mg/L)染毒组及低、中、高剂量姜黄素(100 mg/L亚砷酸钠+25、50、100mg/kg姜黄素)干预组,每组10只。亚砷酸钠采用自由饮用方式进行染毒;姜黄素采用经口灌胃方式染毒,每周3次,连续8周。测量生精小管平均直径;测定大鼠血清睾酮浓度及睾丸生精细胞凋亡指数。结果与对照组比较,亚砷酸钠染毒组大鼠血清睾酮的水平降低,生精小管直径缩小,而睾丸生精细胞凋亡指数升高,差异有统计学意义(P0.01)。与亚砷酸钠染毒组比较,中、高剂量姜黄素干预组大鼠血清睾酮的水平升高,生精小管直径增大,而睾丸生精细胞凋亡指数下降,差异均有统计学意义(P0.05)。且随着姜黄素染毒剂量的升高,大鼠血清睾酮水平和生精小管直径均呈上升趋势,而睾丸生精细胞凋亡指数呈下降趋势。结论姜黄素对砷致大鼠睾丸生殖细胞凋亡具有拮抗作用。     

慢性氟砷染毒对小鼠某些生化指标的影响

[目的]探讨慢性氟、砷染毒对小鼠血液脂质过氧化指标和丙酮酸含量的影响。[方法]昆明种小白鼠120只，随机分成对照、氟染毒、砷染毒和氟砷联合染毒4组，分别自由进食普通、高氟(合F16．844mmol/kg)、高砷(舍As0.400mmol/kg)和高氟高砷(合F16.844mmol/kg；含As0.400mmol/kg)饲料，饲养6个月和12个月后从各组中随机抽出10只小鼠，分别检测其血脂质过氧化物(LPO)和还原型谷胱甘肽(GSH)含量、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶（GSH-Px)活性及丙酮酸合量。[结果]发现慢性氟、砷染毒和氟砷联合染毒均引起血清LPO含量显著升高(P＜0．05或P＜0．01)，全血GSH含量显著降低(P＜0．01)，红细胞S0D和全血GSH—Px活性显著降低(P＜0．05或P＜0．01)，慢性砷染毒和氟砷联合染毒引起全血丙酮酸含量显著升高(P＜0．01)。但各慢性染毒组这些指标的变化程度不同，12个月氟砷联合染毒组全血GSH含量显著低于氟染毒组(P＜0．05)，砷染毒组和氟砷联合染毒组全血GSH-Px活性均显著低于氟染毒组(P＜0．05)。[结论]慢性氟、砷染毒及氟砷联合染毒均引起小鼠血中LPO含量升高、抗氧化能力降低；慢性砷染毒和氟砷联合染毒引起细胞代谢异常；并且氟、砷两毒物对这些作用存在一定的相互影响。     

砷对Keap1抑制HaCaT细胞凋亡及抗氧化水平的影响

目的 基于抑制Kelch样环氧氯丙烷相关蛋白1（Kelch-like ECH-assoicated protein 1,Keap1）基因,研究砷对人永生化角质形成细胞凋亡及抗氧化水平的影响。方法 培养细胞72 h,分为5组：空白对照组、阴性对照（Keap1基因抑制未染砷）、Keap1基因抑制+低砷（2.9 μmol/L）、Keap1基因抑制+中砷（5.8 μmol/L）和Keap1基因抑制+高砷（29.0 μmol/L）组;用流式细胞仪检测细胞凋亡率;用实时荧光定量聚合酶链式反应检测核因子E2相关因子2（nuclear factor erythroid 2-related factor 2,Nrf2）、Keap1 mRNA水平;采用酶联免疫吸附试验检测谷胱甘肽、血红素氧化酶、环氧化酶、S-腺苷甲硫氨酸与同型半胱氨酸蛋白水平。结果 Nrf2和Keap1 mRNA表达不全相等（均有P<0.05）;与阴性对照组相比,低砷组S-腺苷甲硫氨酸和同型半胱氨酸蛋白表达上调（均有P<0.05）,血红素氧化酶蛋白在低、中、高砷组均上调（均有P<0.05）,环氧化酶蛋白在中、高砷组上调（均有P<0.05）,谷胱甘肽蛋白在高砷组上调（F=7.24,P=0.001）。结论 基于Keap1基因抑制,砷暴露上调抗氧化酶活性,提高抗氧化水平,细胞凋亡下降;随着砷剂量增加,Nrf2表达下调,抗氧化水平失衡,细胞凋亡增加。     

亚砷酸钠染毒大鼠肝脏亚细胞砷含量及其砷结合物的分析

给大鼠经口亚慢性染毒亚砷酸钠后,砷主要分布于肝细胞浆,其次为微粒体、线粒体,溶酶体及细胞核;随染毒时间延长各亚细胞器砷含量升高,且在微粒体和线粒体中所占的比例逐渐增大。除核外,各亚细胞器中均有分子量45000和24000蛋白结合砷(HMWP-As和LMWP-As)及6000小分子量砷结合物(LM-As)。微粒体和线粒体中LM-As从无到有,其占各自亚细胞器砷含量的比例逐渐增大,较HMWP-As和LMWP-As的变化似乎更明显,提示LM-As的生成可能与砷对微粒体和线体牡的损伤有关。     

乙苯亚慢性吸入染毒对大鼠肾脏氧化应激损伤和细胞凋亡影响的研究

目的 观察亚慢性吸入染毒乙苯对大鼠肾组织的氧化应激损伤和细胞凋亡的影响.方法 将40只健康3周龄SPF级Sprague-Dawley雄性大鼠随机分为4组,分别为对照(新鲜空气)组和低(433.5 mg/m3)、中(4 335 mg/m3)和高(6 500mg/m3)剂量乙苯染毒组,每组10只.大鼠以笼养方式放入HOPE...     

甲醛慢性吸入暴露致小鼠精子畸形

目的研究甲醛慢性吸入染毒致雄性小鼠生殖细胞遗传毒性。方法 SPF级雄性ICR小鼠40只,随机分为4组:低剂量组、高剂量组、阴性对照组和阳性对照组,每组10只,低、高剂量组染毒剂量分别为1、10 mg/m~3,用静式吸入的方法进行染毒,每天一次,每次2 h,连续染毒20周,阳性对照组给予环磷酰胺。小鼠染毒后继续饲养5周。观察并计算精子畸形率。结果阴性对照组、低剂量组和高剂量组的睾丸脏器系数分别为(0.81±0.13)%、(0.82±0.12)%和(0.78±0.12)%,各组之间差异无统计学意义(P0.05);阴性对照组、阳性对照组、低剂量组和高剂量组的精子畸形率分别为4.1%、6.4%、11.5%和11.3%,与阴性对照组比较,各染毒组精子畸形率明显增加,差异有统计学意义(P0.01);且染毒剂量与精子畸形率之间存在剂量-反应关系(r_s=0.888,P0.01)。结论甲醛慢性吸入染毒可引起小鼠精子畸形率升高,且染毒剂量与精子畸形率之间存在剂量-反应关系。     

Impact of prenatal arsenic exposure on chronic adult diseases

ABSTRACT

Exposure to environmental stressors during susceptible windows of development can result in negative health outcomes later in life, a concept known as the Developmental Origins of Health and Disease (DOHaD). There is a growing body of evidence that exposures to metals early in life (in utero and postnatal) increase the risk of developing adult diseases such as cancer, cardiovascular disease, non-alcoholic fatty liver disease, and diabetes. Of particular concern is exposure to the metalloid arsenic, a drinking water contaminant and worldwide health concern. Epidemiological studies of areas with high levels of arsenic in the drinking water, such as some regions in Chile and Bangladesh, indicate an association between in utero arsenic exposure and the development of adult diseases. Therefore, the need for experimental models to address the mechanism underlining early onset of adult diseases have emerged including the in utero and whole-life exposure models. This review will highlight the epidemiological events and subsequent novel experimental models implemented to study the impact of early life exposure to arsenic on the development of adult diseases. In addition, current research using these models will be discussed as well as possible underlying mechanism for the early onset of disease.

Abbreviations: ALT: alanine aminotransferase; AMI: acute myocardial infarction; AST: aspartate aminotransferase; ATSDR: Agency for Toxic Substances and Disease Registry; CVD: cardiovascular disease; DMA: dimethylarsinate; DOHaD: Developmental Origins of Health and Disease; EPA: U.S. Environmental Protection Agency; ER-α: estrogen receptor alpha; HDL: high-density lipoprotein; HOMA-IR: homeostatic model assessment of insulin resistance; iAs: inorganic arsenic; LDL: low-density lipoprotein; MetS: metabolic syndrome; MMA: monomethylarsonate; NAFLD: non-alcoholic fatty liver disease; PND: postnatal day; ppb: parts per billion; ppm: parts per million; SAM: S-adenosylmethionine; USFDA: United States Food and Drug Administration     

Biochemical effects of chronic exposure to noise in man

Summary Biochemical parameters in 75 normal healthy male subjects exposed to intense noise of 88–107 dB(A) (6–8 h/day) for 10 to 15 years during their work situation have been monitored and compared with 35 normal unexposed subjects. Levels of free cholesterol (P<0.001), -globulin (P<0.01) and cortisol (P<0.01) were found to be significantly higher in the exposed subjects. Significant changes in free cholesterol also altered the ratio of free to esterified cholesterol significantly (P<0.001). The value of the A/G ratio was also lower in the exposed group. Uric acid did not show any change. The study shows that in the exposed group the esterification process of cholesterol was modified. There was an effect on pituitary-adrenal axis as well as host-defence mechanism.     

职业性砷暴露工人尿有机砷和8-羟基脱氧鸟苷水平的相关性

目的评价云南省某砒霜厂工人体内砷的代谢转化与DNA氧化损伤关系。方法选择云南省某砒霜厂一线工人37例（高暴露组）、管理和后勤人员16例（低暴露组）和当地近期无毒物接触史人员28例（对照组）为研究对象,检测尿中有机砷和8-羟基脱氧鸟苷水平,评价砷的代谢转化和DNA氧化损伤相关性。结果高、低暴露组男性尿有机砷分别为（0、48±0．37）mg／L、（0．08±0．05）mg／L,高、低暴露组女性尿有机砷分别为0．11mg／L、（0．30±0．24）mg／L,对照组均低于检出值下限（0．02mg／L）;高、低暴露组和对照组男性尿8-羟基脱氧鸟苷分别为（18．07±11．68）μmol／mol肌酐、（11．79±8．25）μmol／mol肌酐和（10．07±3．04）μmol／mol肌酐,高暴露组高于对照组（P〈0．05）;高、低暴露组和对照组女性尿8-羟基脱氧鸟苷浓度分别为84．35μmol／mol肌酐、（21．27±5．89）μmol／mol肌酐和（14．43±2．58）μmol／mol肌酐,暴露组女性尿8-羟基脱氧鸟苷浓度高于暴露组男性（P〈0．05）。尿中8-羟基脱氧鸟苷浓度随尿中有机砷浓度升高有上升趋势（rs=0．279,P=0．019）。结论砷职业暴露人群存在明显的DNA氧化损伤,对女性损伤更为明显,砷的代谢转化差异可能起关键作用。     

慢性砷暴露对人皮肤角质形成细胞药物转运相关蛋白mRNA表达和砷代谢的影响

目的探讨慢性砷暴露对人皮肤角质形成细胞(human keratinocytes,HaCaT)药物转运蛋白mRNA表达和砷代谢的影响。方法将HaCaT细胞随机分为慢性对照(不予以砷处理)组和慢性砷暴露(100 nmol/L亚砷酸钠染毒28周)组,培养于含10%胎牛血清和1%双抗的培养基中,收集处于对数生长期的细胞,采用实时荧光定量(real-time quantitative PCR)法检测细胞多药耐药相关蛋白mRNA的表达水平。将处于对数生长期的HaCaT对照细胞和慢性砷暴露细胞分别暴露于含终浓度为0(对照)、2.5、5、10、20、30、40、50、60、80、100、150μmol/L亚砷酸钠的培养基中孵育24 h,采用MTS法检测细胞活性。将慢性砷暴露组细胞和对照细胞予以10μmol/L亚砷酸钠处理24 h,采用氢化物发生-原子吸收分光光度法检测细胞砷蓄积和砷排放量。结果与对照细胞相比,慢性砷暴露HaCaT细胞多药耐药相关蛋白ABCC2和ABCC4 mRNA表达水平均升高,差异有统计学意义(P0.05);而ABCC1、ABCC3、ABCC5、ABCG1、ABCG2 mRNA的表达水平均无显著变化。与对照细胞相比,慢性砷暴露HaCaT经各浓度急性砷处理后细胞存活率均升高,差异有统计学意义(P0.05)。与对照细胞相比,10μmol/L亚砷酸钠染毒24 h后,慢性砷暴露细胞内的砷蓄积量降低,而砷排放量升高,差异均有统计学意义(P0.05)。结论慢性砷暴露的HaCaT细胞药物转运蛋白mRNA的表达升高,砷排出能力增强,对砷毒性产生耐受性。     

Comprehensive analysis of the metabolomic characteristics on the health lesions induced by chronic arsenic exposure: A metabolomics study

Early detection of the health lesions induced by chronic arsenic exposure (HLICAE) are crucial to prevent permanent arsenic-induced damage. If HLICAE can be identified in time, appropriate preventive and therapeutic measures may be provided without various avoidable lesions. The present study aims to assess the probability of HLICAE early recognition with metabolomics. Applying a case-control study, 94 participants with HLICAE (cases) and other 94 subjects without HLICAE (controls) were matched with gender and age (±1 year), coming from a previous chronic arsenic exposure cohort. Serum metabolomic profiles were assessed by ultra-high-performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-QTOF-MS) and analyzed with univariate and multivariate statistics. A total of 210 and 364 features were detected in positive and negative ion modes (ESI⁺/ESI^?), respectively. The altered metabolic pathways included lipid and amino acid metabolisms. 28 metabolomics-based biomarkers were significantly associated with HLICAE and provided areas under the curve (AUC, 95% confidence interval) of 0.898 (0.836, 0.960) and 0.908 (0.855, 0.960) in the discovery phase, 78.6% and 86.4% of positive predictive values in the validation phase, in distinguishing HLICAE from controls in ESI⁺/ESI^?, respectively. This study provides novel insights on mechanisms of health effects probably induced by chronic arsenic exposure, and these biomarkers may be applied in HLICAE early detection.     

江西省职业接触砷生物限值研制

目的研制江西省职业接触砷的生物限值。方法对接触砷危害的作业工人进行健康检查和尿砷检测,并结合国内外文献资料进行综合分析。结果对400名接触砷的职业工人进行尿砷测定,结果显示,尿总砷平均值为0．20mg／L,标准差为0．12mg／L,95％上限值为0．40mg／L。36名非职业接触人员尿总砷平均值为0．04mg／L,标准差为O．02mg／L,职业人群与非职业人群差异具有统计学意义（P〈0．01）。职业健康检查结果发现,9人出现砷斑等皮肤样病变。通过工作场所空气中砷及其化合物浓度测定,结合几例砷中毒患者的临床资料和国内外文献,经综合分析,提出江西省尿砷的职业接触限值。结论砷的生物指标较多,经综合分析,课题组认为以尿总砷作为判断指标更为科学合理,建议江西省职业接触砷的生物限值为尿总砷0．40mg／L。     

燃煤砷暴露对人体红细胞免疫黏附功能受损机制的探讨

目的:通过对燃煤型砷中毒患者红细胞免疫黏附功能相关指标的检测,探讨其红细胞免疫黏附功能损伤的可能机制。方法:采用ELISA法测定红细胞CR1(RBC-CR1)分子数量及PCR-RFLP法测定CR1密度基因多态性。结果:砷中毒组RBC-CR1密度基因多态性分布情况:HH型72例(70%)、HL型27例(26.2%)、LL型4例(3.8%)。砷中毒患者RBC-CR1分子数量及各基因型CR1分子数量均明显低于健康对照组,差异均有统计学意义(P<0.01)。结论:RBC-CR1数量减少可能是砷中毒引起红细胞免疫黏附功能受损的重要机制。     

Micronucleus frequency in peripheral blood lymphocytes and buccal mucosa cells of copper smelter workers,with special regard to arsenic exposure

Occupational exposure in copper smelters may produce various adverse health effects including cancer which, according to available epidemiologic data, is associated mainly with exposure to arsenic. Despite a number of well-documented studies reporting an increased risk of cancer among copper smelters workers, the data on genotoxic effects in this industry are scarce. In view of the above, an assessment of micronuclei (MN) frequency in peripheral blood lymphocytes and buccal epithelial cells from copper smelter workers was undertaken. Additionally, the clastogenic/aneugenic effect in lymphocytes was assessed with the fluorescence in situ hybridization (FISH). The study was conducted in three copper smelters in southwestern Poland. The subjects (n = 72) were enrolled among male workers at departments where As concentration in the air was up to at 80 μg/m³. Exposure was assessed by measurement of arsenic concentration in urine and toenail samples. The control group (n = 83) was recruited from healthy male individuals living in central Poland who did not report any exposure to known genotoxins. The results of our study showed a significant increase in MN frequency in peripheral blood lymphocytes and in buccal epithelial cells of smelter workers, compared to the controls (7.96 ± 4.28 vs. 3.47 ± 1.70 and 0.98 ± 0.76 vs. 0.50 ± 0.52, respectively). The FISH technique revealed the presence of clastogenic and aneugenic effects in peripheral blood lymphocytes in both groups. The clastogenic effect was slightly more pronounced in the smelter workers; however, the difference was not statistically significant. The mean arsenic concentrations in urine (total arsenic species) and in toenail samples in the exposed group were 54.04 ± 42.26 μg/l and 7.63 ± 7.24 μg/g, respectively, being significantly different from control group 11.01 ± 10.84 μg/l and 0.51 ± 0.05 μg/g. No correlation between As content in urine or toenail samples and the genotoxic effect was found under study.     

Association between nutritional status and arsenicosis due to chronic arsenic exposure in Bangladesh

The role of nutritional factors in arsenic metabolism and toxicity is not clear. Provision of certain low protein diets resulted in decreased excretion of DMA and increased tissue retention of arsenic in experimental studies. This paper reports a prevalence comparison study conducted in Bangladesh to assess the nutritional status among the chronic arsenic exposed and unexposed population. 138 exposed individuals diagnosed as arsenicosis patients were selected from three known arsenic endemic villages of Bangladesh and age, sex matched 144 unexposed subjects were randomly selected from three arsenic free villages. The mean arsenic concentration in drinking water for the exposed and unexposed population was 641.15 and 13.5 microg L(-1) respectively. Body Mass Index was found to be lower than 18.5, the cut off point for malnutrition, in 57 (41.31%) out of 138 exposed arsenicosis cases and 31 (21.53%) out of 144 unexposed individuals. The crude prevalence ratio (or risk) was 1.92 (95% CI = 1.33-2.78) for poor nutritional status among the arsenicosis cases compared to the unexposed population. The findings of this study add to the evidence that poor nutritional status may increase an individual's susceptibility to chronic arsenic toxicity, or alternatively that arsenicosis may contribute to poor nutritional status.