许昌市某区给水工程工艺设计【含CAD图纸+文档】
收藏
资源目录
压缩包内文档预览：(预览前20页/共54页)
编号：37129807
类型：共享资源
大小：1.46MB
格式：ZIP
上传时间：2020-01-05
上传人：机****料
认证信息
个人认证
高**（实名认证）
河南
IP属地：河南
50
积分
- 关 键 词：
-
含CAD图纸+文档
许昌市
某区
给水
工程
工艺
设计
CAD
图纸
文档
- 资源描述：
-
压缩包内含有CAD图纸和说明书,均可直接下载获得文件，所见所得，电脑查看更方便。Q 197216396 或 11970985
- 内容简介：
-
任务书一、原始依据（包括设计或论文的工作基础、研究条件、应用环境、工作目的等。）根据相关设计资料，确定合理的工艺方案，使给水厂出水水质达到生活饮用水卫生标准（GB5749-2006），并安全输配到用户，满足用户的需求。（1）设计水量：满足最高日供水量 8.5 104m3/d；（2）原水水质：各项指标达到地表水环境质量标准（GB 3838-2002)中的类水质标准；（3）气象水文资料：1）气温：年平均 14.7 ，极端最高_41.9_, 极端最低_-17.4_,最热月月平均最高 32.6 ，最冷月月平均最低 -3.5 。2）降水量：平均年总量 728.3 mm，最大日_177.2_ mm，最大时 64.3 mm。3）相对湿度：最热月平均 79 。4）主导风向： 年最多风向 东南风 ；夏季最多风向：6月 南风 、7月 南风 、8月 东南风 、冬季最多风向：12月 西北风 、1月 西北风 、2月 东南风 、5）风速: 冬季平均： 2.7 m/s、夏季平均 2.2 m/s；6) 平均气压： 996.2 mbar；7）最大冻土深度： 27 cm；8）最大积雪深度： 23 cm；（4）工程地质资料：土壤承载力满足基建设计要求，地下水水位相对标高 -5.0 m；（5）二泵站输水管起端节点水压 50 m。学生在毕业设计过程中熟悉相关的工作方法、工作过程，掌握主体工艺的设计计算和绘图，加强对所学基础知识的应用技能，为日后工作打下坚实基础。二、参考文献1 严煦世、范瑾初主编. 给水工程M. 第4版. 北京：中国建筑工业出版社，19992 中国市政工程东北设计研究院主编. 给水排水设计手册（第1册）常用资料M. 第2版. 北京：中国建筑工业出版社，20003 北京市政工程设计研究总院主编. 给水排水设计手册（第3册）城镇给水M. 第2版. 北京：中国建筑工业出版社，20044 室外给水设计规范（GB500132006）. 中国计划出版社，20065 崔玉川等主编给水厂处理设施设计计算M北京：化学工业出版社，20036 高湘主编给水工程技术及工程实例M北京：化学工业出版社，20027 姜乃昌、陈锦章主编水泵及水泵站M第4版北京：中国建筑工业出版社，19988 张智等主编给水排水工程专业毕业设计指南M北京：中国水利水电出版社，19999 市政工程设计施工系列图集给水排水工程（上、下册），中国建筑工业出版社，200310 王启山主编水工业工程常用数据速查手册M北京：机械工业出版社，200511 严煦世主编给水排水工程快速设计手册（1）给水工程M北京：中国建筑工业出版社，199912 Dr B C Punmia, Ashok Kr Jain, Arun Kr JainWater Supply EngineeringMLaxmi，199513 American Water Works Association，American Society of Civil EngineersWater Treatment Plant Design (4th edition)McGraw-Hill Professional, 200414 其它参考资料三、设计（研究）内容和要求（包括设计或研究内容、主要指标与技术参数，并根据课题性质对学生提出具体要求。）1设计内容要求（1）根据水质、水量、地区条件、施工条件和水厂运行情况、确定净水厂的处理工艺流程。 根据原水水质的各项指标已达到地表水环境质量标准（GB 3838-2002)中的类水质标准；（2）拟定各处理构筑物的设计流量，并根据确定的净水厂位置，选择适宜采用的处理构筑物，确定设计采用的处理构筑物的形式及数量；（3）进行各构筑物的设计计算，确定各构筑物和各主要构件的尺寸并绘制部分计算简图，设计时要考虑到构筑物及其构件施工上的可能性，并符合要求。1）投药及混合根据原水水质、处理要求、货源及其他经济技术条件选定混凝剂品种及投加量，设计溶解池、溶液池，布置加药间及药库，画出草图；确定混合方式，进行混合工艺设计计算和设备选择。2）絮凝、沉淀（或澄清池）絮凝池和沉淀池应同时进行计算和设计，并应注意两者的关系与配合，要使两池之间在高程、水流衔接、深度和池数等方面相互配合。根据设计流量，絮凝池、沉淀池应至少分为独立相同的两组，每组可根据需要分为若干格。也可根据水质情况选用澄清池，并进行设计计算。3）滤池在北方，滤池一般应设在室内，冲洗水泵房应尽可能与滤池合建。4）消毒选定消毒剂并根据水质有关参考资料确定其投加量，投加点应根据水质情况确定。进一步选择投加设备，布置加药间及药库，绘出草图。5）清水池清水池之间要既能互相连通，又能单池运行。清水池应根据水量大小、地形及设计高程而定，由单池容积和设计水深决定水池平面尺寸。（4）根据各构筑物的确定尺寸，确定各构筑物在平面位置上的确切位置，完成平面布置；确定各构筑物间联接管道的位置，管径、长度、材料及附属设施，完成水厂的高程布置。（5）绘制净水厂平面及高程布置图，净水构筑物工艺平、剖面图。（6）二泵站设计计算选泵台数不宜过多，也不宜过少，应能满足各种不同流量及扬程之需要为宜，一般4-7台，尽可能同型号。确定泵站形式，进行泵站设计计算；绘制二泵站工艺图。2设计成果要求（1）设计说明书一份（1.2万字）；参考文献10篇；相关外文文献资料翻译1份（5000汉字）。（2）绘制的图纸折合零号图纸3张，其中至少包括手绘图1张，其内容应满足表1要求。表1 毕业设计绘制图纸要求图纸内容数量及尺寸要求1水厂总平面和高程布置图1张，1号2絮凝和沉淀池平剖面图2张，1号3滤池平剖面图1张，1号4清水池平剖面图1张，1号5送水泵站平剖面图1张，1号指导教师（签字）20xx年2月28日审题小组组长（签字）814Research|Childrens HealthIn 1980, the six New England states discov-ered that PCE (perchloroethylene, tetra-chloroethylene) was leaching into drinkingwater from the inner vinyl lining (VL) ofasbestos cement (AC) water distributionpipes. The vinyl liner, which was introducedin the late 1960s to solve taste and odor prob-lems, had been painted onto the inner surfaceof the pipe in a slurry of PCE and vinyltoluene resin (Piccotex; Johns-ManvilleCorporation, Denver, CO). After drying for48 hr, the pipes were shipped for installation(Demond 1982). Because PCE is a volatilesolvent, it was assumed that most wouldevaporate by the time of pipe installation.However, more than a decade elapsed beforeit was discovered that large quantities of PCEremained in the liner and were slowly leach-ing into the public drinking-water supplies.A substantial number of VL/AC pipeswere installed in the Cape Cod region ofMasssachusetts (Larsen et al. 1983). Becausethe lined pipe was used to replace existingpipe and to extend the water system, contam-ination occurred in an irregular pattern. PCElevels in residential areas of Cape Cod rangedfrom undetectable to 80 g/L along mainstreets and from 1,600 to 7,750 g/L ondead-end streets (Demond 1982). Because itwas prohibitively expensive to replace theVL/AC pipes, a regular schedule of flushingand bleeding was instituted in the most prob-lematic areas to reduce levels to below40 g/L, the suggested no response level in1980 (Demond 1982). The current maxi-mum contaminant level is 5 g/L.Animal experiments suggest an adverseeffect of prenatal exposure to PCE and theclosely related solvent trichloroethylene(TCE) on offspring weight and growth inseveral species (e.g., Elovaara et al. 1979).However, epidemiologic studies have hadinconsistent results (e.g., Bove et al. 1995;Lagakos et al. 1986). We undertook thisstudy to determine the impact of PCE-contaminated drinking water on birth weightand gestational duration using a population-based cohort of Cape Cod children.Materials and MethodsSelection of study population. Children wereeligible for the study if they were born19691983 and their mother was living in aCape Cod town with some VL/AC water dis-tribution pipes at the time of their birth.Children were identified by cross-matching thematernal address on the birth certificate withdata collected from water companies on thelocation, installation year, and diameter of allVL/AC water pipes in the Cape Cod region.Two groups were selected: a) childrenwhose mothers were exposed to PCE-conta-minated drinking water before birth, and b)children whose mothers were unexposedbefore birth. A total of 1,910 children wereinitially designated as “exposed” based on avisual inspection of pipe distribution maps inthe immediate vicinity of the maternaladdress. The initial exposed group included1,862 singleton births and 24 sets of twins.A comparison group initially designated“unexposed” was randomly selected from theremaining resident births. Unexposed childrenwere frequency matched to exposed childrenon month and year of birth. The unexposedgroup of 1,928 children included 1,853 sin-gleton births and 37 sets of twins or triplets.The initial exposure status of a child was con-sidered tentative until survey data on privatewell use became available and more extensiveexposure assessments were completed.We reviewed birth certificates to obtaininformation on the names of the child andhis parents; the parents ages and educationallevels; the date of the mothers last menstrualperiod; and the childs birth weight andgestational age.The study complied with all applicablerequirements of U.S. regulations governing theuse of human subjects in research. The studywas approved by the institutional review boardsof the Massachusetts Department of PublicHealth and Boston University Medical Center,and by the 24A/B/11B Review Committee atthe Massachusetts Department of PublicAddress correspondence to A. Aschengrau, Departmentof Epidemiology, Boston University School of PublicHealth, 715 Albany St., Boston, MA 02118 USA.Telephone: (617) 638-5228. Fax: (617) 638-4458.E-mail: aaschenThis work was supported by grant 5 P42 ES007381from the National Institute of Environmental HealthSciences (NIEHS), National Institutes of Health (NIH). Its contents are solely the responsibility of theauthors and do not necessarily represent the officialviews of NIEHS, NIH.D.O. has testified in personal injury cases involv-ing exposure to tetrachloroethylene and trichloro-ethylene. No such litigation is currently pending.The other authors declare they have no competingfinancial interests.Received 27 April 2007; accepted 4 February 2008.Prenatal Exposure to Tetrachloroethylene-Contaminated Drinking Water andthe Risk of Adverse Birth OutcomesAnn Aschengrau,1 Janice Weinberg,2Sarah Rogers,1Lisa Gallagher,3Michael Winter,4Veronica Vieira,3Thomas Webster,3and David Ozonoff31Department of Epidemiology, 2Department of Biostatistics, 3Department of Environmental Health, and 4Data Coordinating Center,Boston University School of Public Health, Boston, Massachusetts, USABACKGROUND: Prior studies of prenatal exposure to tetrachloroethylene (PCE) have shown mixedresults regarding its effect on birth weight and gestational age.OBJECTIVES: In this retrospective cohort study we examined whether PCE contamination of publicdrinking-water supplies in Massachusetts influenced the birth weight and gestational duration ofchildren whose mothers were exposed before the childs delivery.METHODS: The study included 1,353 children whose mothers were exposed to PCE-contaminateddrinking water and a comparable group of 772 children of unexposed mothers. Birth records wereused to identify subjects and provide information on the outcomes. Mothers completed a question-naire to gather information on residential histories and confounding variables. PCE exposure wasestimated using EPANET water distribution system modeling software that incorporated a fate andtransport model.RESULTS: We found no meaningful associations between PCE exposure and birth weight or gesta-tional duration. Compared with children whose mothers were unexposed during the year of the lastmenstrual period (LMP), adjusted mean differences in birth weight were 20.9, 6.2, 30.1, and15.2 g for children whose mothers average monthly exposure during the LMP year ranged fromthe lowest to highest quartile. Similarly, compared with unexposed children, adjusted mean differ-ences in gestational age were 0.2, 0.1, 0.1, and 0.2 weeks for children whose mothers averagemonthly exposure ranged from the lowest to highest quartile. Similar results were observed for twoother measures of prenatal exposure.CONCLUSIONS: These results suggest that prenatal PCE exposure does not have an adverse effect onthese birth outcomes at the exposure levels experienced by this population.KEY WORDS: birth outcomes, birth weight, drinking-water contamination, gestational duration, lowbirth weight, perchloroethylene, prematurity, tetrachloroethylene. Environ Health Perspect116:814820 (2008). doi:10.1289/ehp.10414 available via / Online 6 February2008Health. All participants gave informed consentbefore taking part in the study.Follow-up and enrollment of subjects.During 20022003, mothers were traced toobtain their current addresses and telephonenumbers. If the mother was deceased, weattempted to locate the father. Letters were sentto all traced parents requesting that they com-plete a self-administered questionnaire. Twofollow-up letters and phone calls were madenonrespondents. As described in Table 1,enrollment patterns were similar for exposedand unexposed subjects.We conducted analyses comparing birthcertificate data on birth weight, gestationalduration, and demographic characteristicsamong participants and nonparticipants. Themean gestational duration was similar amongthe two groups; however, the mean birthweight among nonparticipant children wasabout 100 g lighter than that of participants.Furthermore, although the race and birth yearof nonparticipants were similar to those ofparticipants, nonparticipating mothers wereyounger (mean age, 26.0 vs. 27.5 years), lesseducated (11.3% vs. 3.6% did not graduatefrom high school), and had more prior births(51.1% vs. 24.3% had three or more priorbirths) than participating mothers. These dif-ferences were present for both exposed andunexposed nonparticipants.Questionnaires were sent to all successfullytraced parents to gather information on mater-nal demographic characteristics; prior preg-nancy outcomes; data on smoking, alcoholintake, weight gain, and complications duringeach pregnancy; chronic medical conditions;and other sources of solvent exposure. In addi-tion, information was collected on the familysresidences from 1969 to the birth of the child;the proximity of residences to dry-cleaningestablishments; drinking-water sources; andthe mothers water consumption and bathinghabits at each dwelling. The residential historyincluded the calendar years of residence, exactstreet address, and nearest cross street for allCape Cod residences.Geocoding of residential addresses. Allreported Cape Cod residences were incorpo-rated into a geographic information system(GIS) by geocoding each address using ArcGIS8.1 (ESRI, Redlands, CA). We geocoded theresidences without knowledge of the exposureor birth outcome. Among the 5,324 reportedaddresses, 87.6% had sufficient information tobe geocoded to a parcel. Another 9.6% weregeocoded to the middle of the street or to itsintersection with cross street because the streetnumber was missing. The remaining 2.7 %could not be geocoded with this level of accu-racy, so the 169 associated births wereexcluded from the analysis (Table 1).PCE exposure assessment. Childrenreceived initial exposure designations by amember of our research team (S.R.) who wasfamiliar with the water distribution systemson Cape Cod. The initial designations weredetermined by visually inspecting maps of thepipe network in the immediate vicinity of thebirth certificate address. To determine thefinal exposure designation, we used a leachingand transport model to estimate the mass ofPCE delivered to each residence before andduring the study pregnancy. The model,developed by Webler and Brown for our priorepidemiologic studies (Aschengrau et al.2003; Webler and Brown 1993), estimatesthe amount of PCE entering the drinkingwater using the initial PCE loading in thepipe liner, the pipes age, and the leachingrate of PCE from the liner into the water.The leaching rate of PCE, which declineswith time, was determined from laboratoryexperiments (Demond 1982).The exposure assessment also requires anestimate of water flow, which is a function ofthe pipe configuration and number of waterusers. To estimate flow for the current study,we incorporated the Webler and Brown (1993)algorithm into EPANET water distributionsystem modeling software ().Developed by the U.S. EnvironmentalProtection Agency, this software has beenapplied previously in several epidemiologicinvestigations (e.g., Aral et al. 1996).As a first step, we created a GIS schematicdepicting the water source locations;pipe characteristics; and nodes, which arepoints of water consumption. Information onthe locations, installation dates, and diametersof VL/AC pipes was obtained from localwater departments and the MassachusettsDepartment of Environmental Protection(DEP; Boston, MA). The available informa-tion reflected the water system conditionsaround 1980.Next, we used the schematic to assigneach residence to the closest node on thedistribution system. We assumed that all resi-dences drew the same amount of water andthat the water sources did not change overtime. Typical values for other parameters wereassumed when their variability was low orwhen historical data were absent.The EPANET software incorporated thesedata to simulate the instantaneous flow ofwater through the thousands of pipe segmentsin each towns network and to estimate themass of PCE in grams delivered to subjectsresidences. We estimated three measures ofprenatal PCE exposure: cumulative exposurebefore pregnancy, peak annual exposurebefore pregnancy, and average monthly expo-sure around the time of conception. We esti-mated cumulative exposure before pregnancyby summing the annual mass of PCE thatentered each exposed residence from themove-in year or VL/AC pipe installation year(whichever came later) through the monthand year of the last menstrual period (LMP).We were able to calculate only annual PCEexposures because we knew only the move-inand pipe installation years. We used simplepercentages to estimate PCE exposure for aportion of a year. Peak exposure before preg-nancy was estimated from the highest annualmass of PCE that entered an exposed resi-dence from the move-in year or VL/AC pipeinstallation year (whichever came later) up tothe LMP year. We estimated average monthlyexposure around the time of conception bydividing the annual exposure during the LMPyear by 12. We estimated the LMP from ques-tionnaire or birth certificate data on the gesta-tional duration and birth date. The LMPcould not be estimated for 19 births, and thesewere excluded from the analysis (Table 1).We estimated PCE exposure levels onlyfor children whose mothers had completegeocoded residential histories (Table 1).Children whose mothers reported using a pri-vate well at a Cape Cod residence or who livedPCE-contaminated water and adverse birth outcomesEnvironmental Health PerspectivesVOLUME116 |NUMBER6 | June 2008815Table 1. Selection, enrollment, and exposure status of study births, Cape Cod, Massachusetts, 19691983.Initial exposure statusaExposedUnexposedTotalSelected (no.)1,9101,9283,838Excluded during enrollment (no.)Never located161147308No response306375681Ineligible358Refusal200151351Returned questionnaire (no.)1,2401,2502,490Percent of selected64.964.864.9Percent of located70.970.270.5Excluded during exposure assessment and analysis (no.)Inadequate residential history7396169Multiple birth365389Congenital anomaly present444488Missing last menstrual period10919Available for analysis (no.)1,0771,0482,125Percent of selected56.454.455.4aAfter the more refined EPANET exposure assessment, the exposure designations of 496 children changed, so there were1,353 exposed and 772 unexposed subjects in the final analysis. in a town without VL/AC pipes were assumedto have no PCE exposure during that period.Statistical analysis. We excluded multiplebirths and children born with congenitalanomalies from all analyses (Table 1). Thedata analysis compared the birth weight andgestational duration of exposed and unexposedwomen. For cumulative exposure before preg-nancy, we compared any exposure before theLMP month and year with no exposure beforethe LMP month and year. For peak annualexposure before pregnancy, we compared anyexposure before the LMP year with no expo-sure before the LMP year. Last, for averagemonthly exposure, we compared any exposureduring the LMP year with no exposure duringthe LMP year.We used a locally weighted regressionsmoother (LOESS) to examine the shape ofthe relationship between exposure and theoutcome measures (Hastie and Tibshirani1990). These analyses did not identify anynatural cut points, so we arbitrarily dividedeach exposure measure into quartiles.Analyses examined birth weight and gesta-tional age as continuous variables (in gramsand weeks, respectively) and as the followingdichotomous variables: low birth weight,premature birth, and intrauterine growth retar-dation. Low birth weight was defined as weight 2,500 g, a premature birth was defined asgestation 37 completed weeks, and intrauter-ine growth retardation was defined as a birthweight below the 10th percentile using U.S.race-, sex-, and gestational agespecific cut offsfrom 1970 to 1976 (Williams et al. 1982).Crude analyses compared the means of thecontinuous outcomes and proportions of thecategorical outcomes according to exposure. Inaddition, we conducted generalized estimatingequation (GEE) analyses to account for non-independent outcomes arising from severalAschengrau et al.816Table 2. Distribution of selected characteristics of exposeda,band unexposedbmothers no. (%).aEver exposed before birth. bBased on final exposure designation.CharacteristicExposedUnexposedYear of birth19691973136 (10.1)100 (13.0)19741978446 (33.0)246 (31.9)19791983771 (57.0)426 (55.2)Infants sexMale693 (51.2)378 (49.0)Female660 (48.8)394 (51.0)Age (mean SD)1,353 (27.5 4.5)772 (27.6 4.6)RaceWhite1,291 (95.4)752 (97.4)Nonwhite62 (4.6)20 (2.6)Educational levelLess than high school56 (4.1)21 (2.7)High school graduate48 (35.5)273 (35.4)Some college404 (29.9)253 (32.8)Four year college graduate or higher413 (30.5)225 (29.1)Parity1522 (38.6)304 (39.4)2479 (35.4)282 (36.5)3336 (24.8)178 (23.1)Missing16 (1.2)8 (1.0)Any prior pregnancy lossYes219 (16.2)119 (15.4)No1,118 (82.6)645 (83.5)Missing16 (1.2)8 (1.0)Any prior low-birth-weight infantYes68 (5.0)26 (3.4)No1,261 (93.2)731 (94.7)Missing24 (1.8)15 (1.9)Any prior preterm deliveryYes84 (6.2)42 (5.4)No1,243 (91.9)716 (92.7)Missing26 (1.9)14 (1.8)Interpregnancy intervalFirst live birth526 (38.9)306 (39.6) 12 months133 (9.8)65 (8.4)1223 months234 (17.3)138 (17.9)24 months447 (33.0)256 (33.2)Missing13 (1.0)7 (0.9)Adequacy of prenatal care during pregnancyAdequate989 (73.1)555 (71.9)Intermediate126 (9.3)71 (9.2)Inadequate or no prenatal care8 (0.6)7 (0.9)Missing230 (17.0)139 (18.0)Inadequate weight gain during pregnancyYes121 (8.9)58 (7.5)No1,178 (87.1)680 (88.1)Missing54 (4.0)34 (4.4)Cigarette smoking during pregnancyYes354 (26.2)219 (28.4)No973 (71.9)539 (69.8)Missing26 (1.9)14 (1.8)CharacteristicExposedUnexposedAlcohol consumption during pregnancyYes, during all trimesters345 (25.5)194 (25.1)Yes, during some trimesters176 (13.0)107 (13.9)No799 (59.1)459 (59.5)Missing33 (2.4)12 (1.6)Diabetes before or during pregnancyYes43 (3.2)22 (2.8)No1,283 (94.8)734 (95.1)Missing27 (2.0)16 (2.1)Hypertension or preeclampsia before or during pregnancyYes96 (7.1)63 (8.2)No1,227 (90.7)692 (89.6)Missing30 (2.2)17 (2.2)Bleeding, placental abruption, or previa during pregnancyYes126 (9.3)69 (8.9)No1,212 (89.6)696 (90.2)Missing15 (1.1)7 (0.9)Viral infection during pregnancyYes15 (1.1)8 (1.0)No1,323 (97.8)757 (98.1)Missing15 (1.1)7 (0.9)Cervical incompetence during pregnancyYes24 (1.8)18 (2.3)No1,314 (97.1)747 (96.8)Missing15 (1.1)7 (0.9)History of infertility before pregnancyYes185 (13.7)96 (12.4)No1,162 (85.9)674 (87.3)Missing6 (0.4)2 (0.3)Occupational exposure to solvents before or during pregnancyYes, before or during152 (11.2)77 (10.0)Yes, unknown when24 (1.8)8 (1.0)No1,146 (84.7)666 (86.3)Missing31 (2.3)21 (2.7)Residential proximity to dry cleaning establishmentYes6 (0.4)5 (0.6)No1,330 (98.3)753 (97.5)Missing17 (1.3)14 (1.8)Use of solvent-based spot removersOccasionally or frequently292 (21.6)155 (20.1)Rarely596 (44.1)335 (43.4)Never440 (32.5)262 (33.9)Missing25 (1.8)20 (2.6)Use of professional dry cleaningOnce per month or more194 (14.3)123 (15.9)Less than once per month764 (56.5)405 (52.5)Never321 (23.7)189 (24.5)Missing74 (5.5)55 (7.1)Use of self-service dry cleaningYes126 (9.3)95 (12.3)No1,190 (88.0)659 (85.4)Missing37 (2.7)18 (2.3)PCE-contaminated water and adverse birth outcomesEnvironmental Health PerspectivesVOLUME116 |NUMBER6 | June 2008817children born to the same woman (Liang andZeger 1986; Zeger and Liang 1986). Sixteenpercent of the women had two or more births.The identity and logit links were used for con-tinuous and dichotomous outcomes, respec-tively, while assuming equal correlationbetween birth outcomes from the same mother.Corresponding means, beta coefficients, andodds ratios (ORs) are reported. Ninety-five per-cent confidence intervals (CIs) were used toassess the statistical stability of the associations.Covariates considered for multivariateanalyses were known risk factors for low birthweight or premature delivery or non-drink-ing-water sources of solvent exposure. Onlycovariates of a priori interest or those associ-ated with PCE exposure (OR 1.2 or 0.83)were controlled in the final analyses. Theadjusted birth weight analyses included gesta-tional age, maternal race, educational level,history of a low-birth-weight child, occupa-tional exposure to solvents, use of self-servicedry cleaning, and proximity of any residencesto dry cleaning establishments. Adjusted birthweight analyses were also repeated withoutgestational age and history of low-birth-weight child.Adjusted gestational age analyses includedmaternal race, educational level, prior pretermdelivery, obstetric complications in the currentpregnancy, occupational exposure to solvents,use of self-service dry cleaning, and the prox-imity of any residences to dry cleaning estab-lishments. Adjusted gestational age analyseswere also repeated without history of apreterm delivery. Analyses were also repeatedwith a term for drinking-water source (surfacevs. ground) because of possible confoundingby chlorination by-products present in onetreated surface water supply.Last, we conducted stratified analyses todetermine whether there was effect measuremodification by maternal age at delivery,history of prior pregnancy losses, bottledwater use during pregnancy, tap water useduring pregnancy, and showering habitsduring pregnancy.ResultsA total of 2,125 children were available for thefinal analysis. According to the initial exposuredesignation, there were 1,077 exposed and1,048 unexposed children. After the morerefined EPANET exposure assessment, theexposure designations of 386 children changedfrom unexposed to exposed, and 110 changedfrom exposed to unexposed. Nearly all childrenwho changed their exposure designations fromunexposed to exposed had birth addresses thatwere further downstream from a VL/AC pipethan was originally considered exposed in theinitial visual designation. The EPANET assess-ment of the entire distribution system indicatedthat these downstream locations had potentialfor PCE contamination. On the other hand, allchildren who changed their designations fromexposed to unexposed had mothers whoreported that the birth residence had a privatewell and that they did not receive any publicdrinking water. Thus, the final study popula-tion consisted of 1,353 subjects who were con-sidered exposed before birth and 772 subjectswho were considered unexposed before birth.The characteristics of the exposed andunexposed groups were similar (Table 2).Mothers in both groups were predominantlywhite, and, on average, 27 years old when thechild was born.Comparable proportions in the exposedand unexposed groups smoked cigarettes anddrank alcoholic beverages, and reported medicalconditions and obstetric complications duringthe study pregnancy as well as non-drinking-water sources of solvent exposure. Most womenhad an adequate level of prenatal care.There was wide distribution of PCE levelsencompassing several orders of magnitude forall three exposure measures (Table 3). Themeasures were also highly correlated (pairwiseSpearman correlation coefficients = 0.710.90,p-values 0.001).The exposure measures were based on themass of PCE delivered to a home in each cal-endar year. The annual mass of PCE enteringa home was diluted in an estimated 90,000gallons of water, the annual usage of averagehouseholds in Massachusetts (MassachusettsWater Resources Authority 2003), and only asmall portion of this water was directly con-sumed by the subjects. Using this annual esti-mate of household water use, we converted thePCE mass delivered to a home during preg-nancy to average annual point concentrations,and estimated that the PCE concentrations inthe water entering the homes ranged from 1 g/L to 5,197 g/L. These concentrationsare consistent with actual water-sampling datafrom the time period (Demond 1982).The crude and adjusted analyses showedno consistent pattern of an adverse impact onbirth weight across PCE exposure levels(Tables 4 and 5). In general, birth weights ofexposed infants were greater than those ofunexposed infants. In addition, although thenumber of affected children was small, nomeaningful increases were observed in the ORsfor low birth weight (n = 52) or intrauterinegrowth retardation (n = 136) according to PCEexposure level (data not shown). There wereTable 3. Distribution of cumulative PCE exposure before LMP, peak annual PCE exposure before LMP, andaverage monthly PCE exposure during LMP year among exposed subjects. Cumulative exposure (g)Peak annual exposure (g)Average monthly exposure (g)before LMP month and yearbefore LMP yearduring LMP yearCumulative(n= 1,201)a(n= 955)a(n= 1,106)aMinimum2.8 1041.212 1031.176 10410th percentile8 1025th percentileMedian29.919.80.975th percentile120.063.33.090th percentile334.2161.27.9Maximum3,904.21,770.7147.6aThere were 860 individuals who were exposed both before and during the LMP year. Another 95 individuals wereexposed before the LMP year but were unexposed during the LMP year, and another 246 individuals were exposed duringthe LMP year but were unexposed before the LMP year. Thus, cumulative exposure before the LMP month and yearincludes 1,201 exposed individuals (860 + 95 + 246), peak annual exposure before the LMP year includes 955 exposed indi-viduals (860 + 95), and average monthly exposure during the LMP year includes 1,106 exposed individuals (860 + 246).Table 4. Number of births and crude mean SDfor birth weight and gestational duration by PCEexposure category. No.Mean SDBirth weight (g)Cumulative PCE exposure before LMP month and year75th3013,482 51650th 75th3003,511 55725th 0 25th3003,509 5000 (referent)9243,474 490Peak annual PCE exposure before LMP year75th2393,473 52350th 75th2393,533 55125th 0 25th2383,527 5030 (referent)1,1703,472 495Average monthly PCE exposure during LMP year75th2773,485 49550th 75th2763,483 52125th 0 25th2743,481 4810 (referent)1,0193,481 490Gestational duration (weeks)Cumulative PCE exposure before LMP month and year75th30140.1 2.150th 75th30040.1 2.525th 0 25th30040.2 2.20 (referent)92440.2 2.0Peak annual PCE exposure before LMP year75th23940.1 2.250th 75th23940.1 2.525th 0 25th23840.0 2.10 (referent)1,17040.2 2.0Average monthly PCE exposure during LMP year75th27740.1 1.950th 75th27640.1 2.425th 0 70 min/week) at anexposed residence during the LMP year hadheavier babies with longer gestations than moth-ers who did not take long showers at an exposedresidence. The mean differences in birthweight and gestational duration were 103.4 gand 1.9 weeks, respectively. No effect modifi-cation was seen for showering temperature.DiscussionThe results of this study suggest that prenatalPCE exposure, at the levels experienced by thestudy population, does not have an adverseimpact on birth weight or gestational dura-tion. Compared with unexposed children, theadjusted mean differences in birth weight were20.9, 6.2, 30.1, and 15.2 for children whosemothers average monthly PCE exposureduring the LMP year ranged from the lowestto highest quartile. Similarly, the adjustedmean differences in gestational age were 0.2,0.1, 0.1, and 0.2 weeks for children whosemothers average monthly PCE exposure dur-ing the LMP year ranged from the lowest tohighest quartile. The results were similar whencumulative and peak exposure before preg-nancy were examined.These results are likely affected by expo-sure misclassification. Because individualexposure measurements were unavailable, weestimated historical PCE exposures using aleaching and transport model (Webler andBrown 1993) that estimated the mass of PCEdelivered to each residence. Nevertheless,results from a validation study indicate rea-sonable correlation between exposure esti-mates based on the WeblerBrown algorithmand PCE concentrations in historical watersamples (Spearman correlation coefficient =0.48, p 0.0001; Spence LA, Aschengrau A,Gallagher L, Webster T, Heeren T, OzonoffD, unpublished data). The EPANET software estimated theamount of PCE that entered the home, so wedo not know each subjects precise exposurefrom showering, bathing, and tap-water con-sumption, which can result in dermal, oral,and inhalation exposure (Vieira et al. 2005).Although we obtained information on moth-ers water consumption and bathing habitsbefore and during pregnancy, this informa-tion was difficult to recall accurately becauseit occurred so long ago. Thus, exposure mis-classification is also likely from unmeasuredor poorly measured physical and behavioralfactors that influenced exposure. Poor recallalso made it difficult to detect effect measuremodification by drinking and bathing habits.Exposure misclassification may also stemfrom our measures of prenatal PCE exposure,particularly cumulative exposure which com-bined both dose and duration. However, ouranalyses of peak prenatal exposure, whichfocused only on dose, did not find any adverseimpacts on birth weight or gestational duration.Even though exposure misclassification isprobable, the preliminary results of an ongo-ing validation study suggest that its magnitudeis modest, particularly given the quartile expo-sure categories used in the current analysis.Nevertheless, we cannot rule out a smallincreased risk of prenatal PCE exposure on theoutcomes under study, given the likely down-ward bias of the misclassification. Last, it is pos-sible that a null result was observed for birthweight and gestational duration because PCEexposure can lead to spontaneous abortion.The current study has numerous strengths,including a relatively large sample size with awide range of exposure levels, data on birthweight and gestational duration from birthcertificates, and information on manyconfounding variables. In addition, levels ofAschengrau et al.818Table 5. MultivariateaGEE analysis of birth weight and gestational duration by PCE exposure category.No.SD95% CIBirth weight (g)Cumulative PCE exposure before LMP month and year75th28128.533.637.4 to 94.450th 75th27953.734.313.6 to 120.925th 0 25th 27942.131.820.3 to 104.50 (referent)867Peak annual PCE exposure before LMP year75th22414.636.055.9 to 85.150th 75th220 to 131.225th 0 25th230 to 138.70 (referent)1,089Average monthly PCE exposure during LMP year75th25415.232.748.9 to 79.350th 75th25730.133.335.2 to 95.425th 0 25th26220.931.741.2 to 82.90 (referent)958Gestational duration (weeks)Cumulative PCE exposure before LMP month and year75th28 to 0.150th 75th27 to 0.225th 0 25th 28 to 0.20 (referent)872Peak annual PCE exposure before LMP year75th22 to 0.250th 75th2 to 0.225th 0 25th230 to 0.10 (referent)1,096Average monthly PCE exposure during LMP year75th25 to 0.150th 75th25 to 0.225th 0 25th 26 to 0.10 (referent)96325th, 50th, and 75th are percentiles.aBirth weight adjusted for gestational age, maternal race, educational level, history of a low-birth-weight child, occupa-tional exposure to solvents, use of self-service dry cleaning, and proximity of any residences to dry cleaning establish-ments. Gestational age adjusted for maternal race, educational level, history of a preterm delivery; complications such asplacenta previa, placental abruption, and cervical incompetence; occupational exposure to solvents, use of self-servicedry cleaning, and the proximity of any residences to dry-cleaning establishments.other measured drinking-water contaminantswere low (Swartz et al. 2003). Trihalomethanelevels were low because only one surface-watersource in this region was treated with chlorina-tion. Furthermore, the results were unchangedwhen drinking-water source (surface vs.ground) was controlled. Although nonpartici-pating mothers were younger, less educated,and had lighter babies than participatingmothers, these differences were present forboth exposed and unexposed nonparticipants,so it is unlikely they biased the current results.Animal experiments suggest that anadverse effect on birth weight and size occursin several species after prenatal exposure toPCE and the closely related solvent TCE(Bross et al. 1983; Dorfmueller et al. 1979;Elovaara et al. 1979; Healy et al. 1982;Saillenfant et al. 1995; Schwetz et al. 1975).Detrimental effects were seen only at highexposure levels in some experiments e.g.,1,800 ppm TCE (Dorfmueller et al. 1979)but were observed at relatively low levels inothers e.g., 1 M TCE (Bross et al. 1983);100 ppm TCE (Healy et al. 1982).Epidemiologic studies of women exposedoccupationally to solvents including drycleaning and degreasing agents have inconsis-tent results regarding an adverse effect onbirth weight and gestational duration. Eightstudies of birth weight found null results(Axelsson et al. 1984; Bosco et al. 1987;Hewitt and Tellier 1998; Laslo-Baker et al.2004; McDonald et al. 1987; Olsenand Rachootin 1983; Seidler et al. 1999;Windham et al. 1991), whereas four studiesobserved 1.5- to 2.7-fold increases in the riskof low birth weight or moderate declines inmean birth weight (82 to 168 g) (Ha et al.2002; Hewitt and Tellier 1998; Khattak et al.1999; Lipscomb et al. 1991). Three previousoccupational studies found null associationsbetween prenatal solvent exposure and gesta-tional duration (Ha et al. 2002; Laslo-Bakeret al. 2004; Savitz et al. 1996), whereas fourstudies found positive associations, rangingfrom 1.3- to 3.1-fold increases in the risk ofpreterm delivery (Hewitt and Tellier 1998;Khattak et al. 1999; Lipscomb et al. 1991;Savitz et al. 1989).The occupational studies are difficult tocompare with the present study because mostworkers were exposed to relatively high dosesof a variety of solvents, solvent mixtures, andother noxious chemicals. Furthermore, dataon important confounding factors such as cig-arette smoking were often unavailable, andthe numbers of exposed women were quitesmall, thereby reducing the ability of thesestudies to detect even a modest effect.It is also difficult to generalize results seenamong women exposed occupationally to sol-vents to those in the general populationbecause of differences in socioeconomic statusand reproductive history. For example,women who either cannot find work or donot have a monetary incentive to work arenot represented in the occupational studies.In addition, women whose pregnancy historyconsists only of adverse outcomes such asspontaneous abortions are more likely toremain in the work force, whereas those whohave had live-born children are more likely todrop out (Joffe 1985).Prior community-based epidemiologicstudies of solvent contaminated drinkingwater are more comparable to the currentinvestigation. All prior drinking-water studieson PCE and TCE contamination had nullfindings for gestational duration (Bove et al.1995; Massachusetts Department of PublicHealth 1996; Sonnenfeld et al. 2001).Although three prior studies observed nomeaningful increases in the risk of low birthweight (Lagakos et al. 1986; Rodenbeck et al.2000; Sonnenfeld et al. 2001), two studiesobserved increases in the risk of very low birthweight (defined as 1,500 g) (Bove et al.1995; Rodenbeck et al. 2000). In addition,some studies reported adverse effects in cer-tain subgroups. These included an increasedrisk of growth retardation among womenwith moderate and high third-trimester sol-vent exposure (Massachusetts Department ofPublic Health 1996), and decreased birthweights among women 35 years of age(adjusted mean difference = 130 g; 90% CI,236 to 23) and women with a history oftwo or more fetal losses (104 g; 90% CI,174 to 34) (Sonnenfeld et al. 2001). In ourstudy, the occurrence of very low birth weightwas too low to conduct meaningful analyses,and the exposure data were not detailedenough to conduct analyses by trimester. Inaddition, we did not observe effect measuremodification by maternal age or a history ofpregnancy losses.Drinking-water studies with positive asso-ciations had water contaminant levels rangingfrom 14 to 215 g/L PCE (Bove et al. 1995;Sonnenfeld et al. 2001), and from 55 to 107g/L TCE (Bove et al. 1995; Rodenbeck et al.2000). In comparison, PCE levels in residen-tial water supplies of Cape Cod in 1980ranged from undetectable to 780 g/L, with amean of 45 g/L (Spence LA, Aschengrau A,Gallagher L, Webster T, Heeren T, OzonoffD, unpublished data). Thus, it is likely thatsome of our subjects had greater exposuresthan seen in the studies from New Jersey,North Carolina, and Arizona.Demographic differences between ourstudy population and that of several priorstudies may account for the diverse findings.The other study populations had substantialproportions of women who were black orHispanic, had low educational levels, and hadinadequate levels of prenatal care. (Bove et al.1995; Rodenbeck S, personal communica-tion; Rodenbeck et al. 2000; Sonnenfeld et al.2001). In contrast, as described in Table 2,mothers in our study were predominantlywhite, well educated, and connected to prena-tal care. These characteristics are consistentwith the low rates of low birth weight andvery low birth weight seen in our populationcompared with rates in the general population(National Center for Health Statistics 2004),and may weaken the adverse effects of prena-tal exposure to contaminated drinking water.In summary, we found no associationbetween prenatal PCE exposure and birthweight and gestational duration. Our resultssuggest that prenatal PCE exposure does nothave an adverse effect on these outcome mea-sures at the levels experienced by our studypopulation. Given the likelihood of exposuremisclassification, we cannot rule out a smalladverse effect of PCE on these birth outcomes.Furthermore, because the occurrence of verylow birth weight was very low in our popula-tion, this study cannot provide evidence for oragainst an association with this outcome. Last,it is possible that our results are not generaliz-able to more vulnerable populations. BecausePCE remains a commercially ubiquitous sol-vent and common contaminant of drinking-water supplies (Agency for Toxic Substancesand Disease Registry 1997; Moran et al.2007), it is important to understand its effecton women and their pregnancies.REFERENCESAgency for Toxic Substances and Disease Registry. 1997.Toxicological Profile for 1,1,2,2-Tetrachloroethylene.Atlanta, GA:Agency for Toxic Substances and DiseaseRegistry. Aral MM, Maslia ML, Ulirsch GV, Reyes JJ. 1996. Estimatingexposure to volatile organic compounds from municipalwater-supply systems: use of a better computationalmodel. Arch Environ Health 51(4):300309.Aschengrau A, Rogers S, Ozonoff D. 2003. Perchloroethylene-contaminated drinking water and the risk of breast can-cer: additional results from Cape Cod, Massachusetts.Environ Health Perspect 111:167173.Axelsson G, Lutz C, Rylander R. 1984. Exposure to solvents andoutcome of pregnancy in university laboratory employees.Br J Ind Med 41:305312.Bosco MG, Figa-Talamanca I, Salerno S. 1987. Health andreproductive status of female workers in dry cleaningshops. Int Arch Occup Environ Health 59:295301.Bove FJ, Fulcomer MC, Klotz JB, Esmart J, Dufficy EM, SavrinJE. 1995. Public drinking water contamination and birthoutcomes. Am J Epidemiol 141:850862.Bross G, DiFranceisco D, Desmond ME. 1983. The effects oflow dosages of trichloethylene on chick development.Toxicology 28:283294.Demond AH. 1982. A Source of Tetrachloroethylene in theDrinking Water of New England: An Evaluation of Toxicityof Tetrachloroethylene and the Prediction of its LeachingRates from Vinyl-lined Asbestos-cement Pipe MS Thesis.Cambridge, MA:Massachusetts Institute of Technology.Dorfmueller MA, Henne SP, York RG, Bornschein RL, MansonJM. 1979. Evaluation of teratogenicity and behavioral toxi-city with inhalation exposure of maternal rats totrichloroethylene. Toxicology 14:153166.Elovaara E, Hemminki K, Vainio H. 1979. Effects of methylenechloride, trichloroethane, trichloroethylene, tetrachlor-ethylene and toluene on the development of chickembryos. Toxicology 12:111119.PCE-contaminated water and adverse birth outcomesEnvironmental Health PerspectivesVOLUME116 |NUMBER6 | June 2008819Ha E, Cho S-I, Chen D, Chen C, Ryan L, Smith TJ, et al. 2002.Parental exposure to
- 温馨提示:
1: 本站所有资源如无特殊说明，都需要本地电脑安装OFFICE2007和PDF阅读器。图纸软件为CAD,CAXA,PROE,UG,SolidWorks等.压缩文件请下载最新的WinRAR软件解压。
2: 本站的文档不包含任何第三方提供的附件图纸等，如果需要附件，请联系上传者。文件的所有权益归上传用户所有。
3.本站RAR压缩包中若带图纸，网页内容里面会有图纸预览，若没有图纸预览就没有图纸。
4. 未经权益所有人同意不得将文件中的内容挪作商业或盈利用途。
5. 人人文库网仅提供信息存储空间，仅对用户上传内容的表现方式做保护处理，对用户上传分享的文档内容本身不做任何修改或编辑，并不能对任何下载内容负责。
6. 下载文件中如有侵权或不适当内容，请与我们联系，我们立即纠正。
7. 本站不保证下载资源的准确性、安全性和完整性, 同时也不承担用户因使用这些下载资源对自己和他人造成任何形式的伤害或损失。
人人文库网所有资源均是用户自行上传分享，仅供网友学习交流，未经上传用户书面授权，请勿作他用。
川公网安备: 51019002004831号