多环芳烃暴露生物标志物羟基多环芳烃检测方法的研究进展

多环芳烃(PAHs)是一类普遍存在于环境中的持久性有机污染物,长期暴露可引发肺癌、皮肤癌等恶性肿瘤。而PAHs的代谢物——单羟基多环芳烃(OH-PAHs)可以作为暴露生物标志物综合评价人体对PAHs的暴露水平,从而吸引众多研究人员对OH-PAHs检测方法的研究。笔者介绍了生物标志物以及选用OH-PAHs作为生物标志物的意义,系统综述了OH-PAHs的各种检测方法,包括高效液相色谱法、液相色谱-质谱(气相色谱-质谱)联用技术、同步荧光光谱分析法、毛细管区带电泳法、酶联免疫法和电化学法,并对其检测方法的发展趋势进行了评价和展望。     

Progress on Detection Methods for Hydroxyl Polycyclic Aromatic Hydrocarbons as a Biomarker of Exposure to Polycyclic Aromtic Hydrocarbons

多环芳烃(PAHs)是一类普遍存在于环境中的持久性有机污染物,长期暴露可引发肺癌、皮肤癌等恶性肿瘤.而PAHs的代谢物——单羟基多环芳烃(OH-PAHs)可以作为暴露生物标志物综合评价人体对PAHs的暴露水平,从而吸引众多研究人员对OH-PAHs检测方法的研究.笔者介绍了生物标志物以及选用OH-PAHs作为生物标志物的意义,系统综述了OH-PAHs的各种检测方法,包括高效液相色谱法、液相色谱-质谱(气相色谱-质谱)联用技术、同步荧光光谱分析法、毛细管区带电泳法、酶联免疫法和电化学法,并对其检测方法的发展趋势进行了评价和展望.     

吸烟对焦炉工人尿中10种多环芳烃代谢物浓度的影响

目的 研究吸烟对焦炉作业工人尿中多环芳烃(PAHs)代谢物浓度的影响.方法 采用高效液相色谱法检测工人工作环境中颗粒物载带上的PAHs浓度;通过职业健康体检和问卷调查的方式收集某焦化厂1401名男性焦炉工人的职业信息,并采集尿液;使用气相色谱-质谱联用仪测定尿样中10种羟基多环芳烃代谢产物(OH-PAHs)的浓度.按照工作岗位和工作环境PAHs浓度的差异分成对照组、低暴露组、中暴露组和高暴露组4组,采用协方差分析分别比较各组吸烟者与不吸烟者尿中10种OH-PAHs的浓度差异.结果 工作环境中16种PAHs的检测结果均显示高暴露组＞中暴露组＞低暴露组＞对照组,高暴露组的浓度明显高于对照组、低暴露组和中暴露组,差异有统计学意义(P＜0.05).在对照组、低暴露组、中暴露组和高暴露组中,吸烟者尿中1-羟基萘(1-OHNa)和2-羟基萘(2-OHNa)的浓度明显高于不吸烟者,差异有统计学意义(P＜0.05);4个组中,吸烟者的1-羟基芘(1-OHP)浓度与不吸烟者的差异无统计学差异(P＞0.05).结论 在焦炉作业人群中,尿中1-OHNa和2-OHNa可以作为评价吸烟对工人尿中OH-PAHs浓度影响的生物标志物.     

尿中多环芳烃羟基代谢物分析方法研究进展

多环芳烃(PAHs)是广泛分布于环境及职业场所的致癌性化合物,PAHs的生物标志物可以准确反映人体对PAHs的内暴露情况,PAHs在代谢物中主要以OH-PAHs与葡萄糖醛酸结合物的形式存在,本文对尿中OH-PAHs的不同前处理过程与分析方法分别进行了比较与阐述。 更多还原     

人尿液中10种羟基多环芳烃同时检测

多环芳烃(PAHs)是一类具有三致作用并在全球广泛分布的有机污染物,对人体健康具有潜在危害^〔1〕。PAHs可通过呼吸道、皮肤接触、消化道等多种暴露途径进入人体,经体内代谢成羟基多环芳烃(OH-PAHs),并以葡萄糖醛酸、硫磺酸结合物的形式主要通过尿液排泄^〔2〕。目前,国际上广泛利用尿液中OH-PAHs作为生物标志物,对PAHs在人体内的暴露水平进行综合评价^〔3〕。高效液相色谱(HPLC)因具有快速、灵敏、易推广等特点,被普遍用于尿液中OH-PAHs的分析。迄今,使用HPLC同时检测尿液OH-PAHs一般在2~8种^〔4,5〕。     

天津市老年人群大气多环芳烃暴露与尿中多环芳烃羟基代谢物的关联研究

目的 同时测定尿中多种羟基多环芳烃(OH-PAHs),以期发现适于联合评价多环芳烃(PAHs)内暴露水平的OH-PAHs.方法 于2011年6月采集112名研究对象24 h的个体颗粒物暴露和晨尿样本,用气相色谱-质谱法检测个体颗粒物样本载带的PAHs及尿样中OH-PAHs.结果 尿样中共检出7种OH-PAHs,其中1-羟基萘(1-OHNap)检出浓度最高[(20.54±28.94) μmol/mol Cr],1-羟基芘(1-OHP)检出浓度最低[(0.73±0.63) μmol/mol Cr].各种OH-PAHs的浓度按照1-OHNap＞9-羟基芴(9-OHFlu) ＞2-羟基萘(2-OHNap)＞3-羟基芴(3-OHFlu)＞2-羟基芴(2-OHFlu)＞6-羟基屈(6-OHChr)＞1-OHP的顺序递减,性别和吸烟对研究对象尿液中OH-PAHs的浓度没有显著影响.总羟基萘(∑OHNap)与1-OHNap具有良好的相关性(r=0.948),总羟基芴(∑OHFlu)与9-OHFlu具有良好的相关性(r=0.975),1-OHNap与颗粒物载带的萘的相关性优于2-OHNap,9-OHFlu与颗粒物载带的芴的相关性优于3-OHFlu和2-OHFlu,∑OHNap、∑OHFlu和6-OHChr与1-OHP的r值分别为0.427、0.543和0.655.结论 仅用1-OHP作为机体PHAs的生物标志物并不能反映人体的内暴露水平,1-OHNap和9-OHFlu对∑OHNap和∑OHFlu暴露水平有较好的预测效果;1-OHNap、9-OHFlu结合1-OHP联合测定可以更为准确和全面地评价PAHs内暴露水平.     

被动吸烟对孕妇尿中4种多环芳烃代谢物浓度的影响

[目的] 以尿中2-羟基萘(2-NAP)、2-羟基芴(2-FLU)、9-羟基菲(9-PHE)和1-羟基芘(1-PYR)作为生物标志物,评价太原市孕妇体内多环芳烃(PAHs)暴露水平,探讨被动吸烟对其浓度的影响. [方法]2009年4月-2010年4月,抽取太原市某医院住院分娩孕妇287人,对其工作生活环境等情况进行问卷调查.将符合纳入标准的264名孕妇根据被动吸烟指数等级分为3组:0、1～49、≥50组,收集各组产前尿样,利用高效液相色谱-荧光检测法测定尿中4种PAHs的羟基代谢产物(OH-PAHs)水平. [结果]符合纳入标准的孕妇尿样中均可检测到2-羟基萘、2-羟基芴、9-羟基菲和1-羟基芘,浓度中位数分别为0.47、0.24、0.23和0.10 μg/mmolCr.除9-羟基菲外,3组尿中2-羟基萘、2-羟基芴、1-羟基芘的差异均有统计学意义(P＜0.05);多元线性回归分析显示,被动吸烟、使用煤炉、采暖期、汽修厂加油站是影响孕妇尿中4种OH-PAHs水平的主要因素. [结论]被动吸烟可以增加孕妇尿中4种OH-PAHs含量,其中2-羟基萘可以作为反映被动吸烟对孕妇体内多环芳烃暴露水平影响的最佳指标.     

焦化作业工人多环芳烃暴露与生物监测结果分析

对焦化厂不同工作岗位工人多环芳烃(PAHs)污染暴露及其生物监测结果进行了分析。采用个体采样器采集样品,高效液相色谱检测工人接触空气中的日均PAHs浓度,同时收集工人的尿液,对其中PAHs代谢产物进行分析。分析结果表明,各岗位工人PAHs日平均暴露浓度为9.43~40.12μg/m3;各岗位工人尿中1-羟基芘(1-OH-P)日排出量为1.04~11.10μg,9-羟基苯并(a)芘(9-OH-BaP)日排出量为0.026~0.042μg;3-羟基苯并(a)芘(3-OH-BaP)日排出量为0.072~0.192μg;焦化厂岗位工人PAHs暴露浓度和尿中PAHs代谢产物之间线性相关关系具有显著意义。     

焦化厂工人尿中多环芳烃代谢物与神经行为功能改变的关系

目的  探讨某焦化厂工人尿中多环芳烃(polycyclic aromatic hydrocarbons, PAHs)代谢物与神经行为功能改变的关系。方法 2017年对山西省某焦化厂的672名工人进行基本情况调查、神经行为功能测试和尿中多环芳烃羟基代谢物(polycyclic aromatic hydrocarbons hydroxyl metabolites, OH-PAHs)的检测;于2021年进行随访,共461名工人完成神经行为功能测试。采用WHO推荐的神经行为测试组合(neurobehavioral core test battery, NCTB)对工人神经行为功能进行测试;使用高效液相色谱-串联质谱联用(high performance liquid chromatography with tandem mass spectrometry, HPLC-MS/MS)检测尿中OH-PAHs和尿中可替宁。使用广义线性模型和广义估计方程分析工人尿中OH-PAHs与神经行为功能的关系。结果  研究对象基线年龄为34(30, 46)岁,男性占比69.2%。纵向研究中,2-羟基萘(2-hydroxynaphthalene, 2-OHNAP)高暴露组的顺序数字跨度(β=-0.50, 95% CI: -0.81~-0.18, P=0.002)和总数字跨度得分(β=-0.77, 95% CI: -1.38~-0.16, P=0.014)降低;2-羟基芴(2-hydroxyfluorene, 2-OHFLU)高暴露组的平均反应时间明显延长(β=26.90, 95% CI: 7.86~45.93, P=0.006),习惯手提转捷度(β=-1.30, 95% CI: -2.43~-0.17, P=0.024)和非习惯手提转捷度得分(β=-1.19, 95% CI: -2.23~-0.15, P=0.025)降低。结论  长期暴露于高浓度多环芳烃环境中会导致焦化厂工人神经行为功能降低。     

大气细颗粒物多环芳烃暴露对健康人尿中羟基代谢物和氧化应激水平的影响

目的 研究大气颗粒物（PM2.5）及多环芳烃暴露与人体内羟基代谢物的关系,并探讨其对健康人群氧化应激水平的影响。方法 招募46名在校大学生,采用定组研究的方法,于2015夏季和冬季对招募对象进行2次随访,采集研究对象尿样并测定尿中羟基代谢物和8 - 羟基脱氧鸟苷。结果 PM2.5、∑PAHs浓度和温度在夏季和冬季的差异有统计学意义（P＜0.05）;而相对湿度（RH）间差异无统计学意义;在夏季时,2 - OHFlu、3 - OHPhe、1 - OHPhe和1 - OHPyr浓度依次为0.25、0.16、0.13、0.08 μmol/mol Cr;而冬季浓度依次为0.63、0.73、0.40、0.42 μmol/mol Cr,经配对t检验,2组间差异均有统计学意义。而8 - OHdG虽然在冬季略高于夏季,但2组间差异无统计学意义。经Spearman 相关分析,4种OH - PAHs与∑PAHs均有较强相关性,8 - OHdG、PM2.5、∑PAHs及OH - PAHs无相关性。结论 细颗粒物PM2.5及多环芳烃暴露对人体羟基代谢物水平有影响,冬季羟基代谢物水平高于夏季,而对8 - OHdG的影响不显著。     

石化企业周边中老年居民的多环芳烃内暴露水平研究

目的了解我国石化企业周边居民体内多种多环芳烃（PAHs）的内暴露水平与分布特征。方法于2012年7月选取我国南方某大型石化企业,采用系统抽样法在石化企业周边收集到当地≥45岁居民的尿样。采用快速液相色谱-三重四级杆串联质谱仪检测多环芳烃羟基代谢物（OH—PAHs）。结果本研究共调查165名≥45岁石化企业周边居民,男、女性分别为81、84人,以45～64岁居民为主,占62．82％（102／165）。职业构成主要以农民为主,占49．09％（81／165）。检出2-羟基萘（2-OHN）、1-羟基萘（1-OHN）、2-羟基芴＋3-羟基芴（2-＋3-OHF）、2-羟基菲（2-OHPhe）、3-羟基菲（3-OHPhe）、4-羟基菲（4-OHPhe）、1-羟基菲＋9-羟基菲（1-＋9-OHPhe）和1-羟基芘（1-OHP）10种OH-PAHs,其浓度的中位数分别为：1．83、1．34、0．51、0．14、0．21、0．07、0．69、0．25μmol／mol肌酐,除2-OHN和1-＋9-OHPhe之间无相关性,其他各OH-PAHs间均呈正相关关系（P〈0．05或P〈0．01）,相关系数在0．20～0．76之间。除OHPhes外,吸烟人群体内的其他OH-PAHs含量均高于不吸烟人群（P〈0．05或P〈0．01）。结论石化厂区域中老年居民尿液样本中以总羟基萘（1-OHN和2-OHN）为主,这与石化厂多环芳烃的污染主要是低环的化合物为主一致。     

多环芳烃暴露与饮酒影响非吸烟人群心理健康状况的交互作用

目的  探讨多环芳烃(polycyclic aromatic hydrocarbons, PAHs)暴露与饮酒影响非吸烟人群心理健康的独立与交互作用。 方法  本研究对513名广西壮族自治区(简称广西)某大型企业非主动吸烟员工进行问卷调查、心理健康评估。使用一般心理健康问卷量表评估研究对象心理健康状况;尿中羟基多环芳烃(hydroxypolycyclic aromatic hydrocarbons, OH-PAHs)水平作为PAHs的内暴露指标;采用logistic回归分析模型和广义线性模型分析PAHs与饮酒的独立和交互作用对心理健康状况的影响。 结果  本组研究对象年龄为(39.60±6.60)岁,44.2%的职工饮酒,饮酒者多为未婚、男性、有二手烟暴露(均有P < 0.05)。logistic回归分析模型结果显示,总体研究对象尿液1-羟基萘(1-hydroxynaphthalene, 1-OHNAP)和总羟基萘(total hydroxynaphthalene, ∑OHNAPs)浓度增加会引起人群心理健康状况不良的发生风险增高(OR=1.23, 95% CI：1.01~1.49;OR=1.10,95% CI：1.00~1.21;均有P < 0.05)。交互分析结果显示,与不饮酒组及低水平尿OH-PAHs相比,尿中1-OHNAP、2-羟基萘(2-hydroxynaphthalene, 2-OHNAP)、∑OHNAPs和总羟基多环芳烃(total hydroxypolycyclic aromatic hydrocarbons, ∑OHPAHs)浓度与饮酒的交互作用增加中老年人发生心理健康状况不良的风险(OR=3.91, 95% CI: 1.01~15.11; OR=3.69, 95% CI: 1.05~12.98; OR=1.96, 95% CI: 1.01~3.80; OR=1.73, 95% CI: 1.06~2.93;均有P_int＜0.05)。 结论  PAHs暴露是非吸烟人群心理健康状况不良的危险因素,并且饮酒会增加PAHs对非吸烟中老年人不良心理健康状况的发生风险。     

Concentration and profile of 22 urinary polycyclic aromatic hydrocarbon metabolites in the US population

Urinary monohydroxy polycyclic aromatic hydrocarbons (OH-PAHs) are a class of PAH metabolites used as biomarkers for assessing human exposure to PAHs. The Centers for Disease Control and Prevention's National Health and Nutrition Examination Survey (NHANES) uses OH-PAHs to establish reference range concentrations for the US population, and to set benchmarks for future epidemiologic and biomonitoring studies. For the years 2001 and 2002, 22 OH-PAH metabolites were measured in urine specimens from 2748 NHANES participants. Percentages of samples with detectable levels ranged from nearly 100% for metabolites of naphthalene, fluorene, phenanthrene, and pyrene, to less than 5% for metabolites from parent compounds with higher molecular weight such as chrysene, benzo[c]phenanthrene, and benz[a]anthracene. The geometric mean for 1-hydroxypyrene (1-PYR)—the most commonly used biomarker for PAH exposure—was 49.6 ng/L urine, or 46.4 ng/g creatinine. Children (ages 6–11) generally had higher levels than did adolescents (ages 12–19) or adults (ages 20 and older). Model-adjusted, least-square geometric means for 1-PYR were 87, 53 and 43 ng/L for children, adolescents (ages 12–19) and adults (ages 20 years and older), respectively. Log-transformed concentrations for major detectable OH-PAHs were significantly correlated with each other. The correlation coefficients between 1-PYR and other metabolites ranging from 0.17 to 0.63 support the use of 1-PYR as a useful surrogate representing PAH exposure.     

超高效液相色谱串联质谱检测生物样本中多环芳烃

目的建立高灵敏度的超高效液相色谱-串联质谱(UPLC-MS/MS)分析方法,用于检测生物样本中痕量多环芳烃(PAHs),包括血浆中3种致癌性多环芳烃苯并(a)芘(BaP)、苯并(g,h,i)苝[B(g,h,i)P]、二苯并(a,h)蒽[DB(a,h)A],及尿液中三种羟基多环芳烃代谢产物2-羟基萘(2-OHN)、2-羟基芴(2-OHF)、1-羟基芘(1-OHP)。方法血浆经饱和氯化钠过夜盐析,尿液经β-葡糖苷酸酶水解,固相萃取后,用UPLC-MS/MS分析。结果血浆中3种致癌性多环芳烃在0.5～100μg/L浓度范围内呈良好的线性关系,线性相关系数均大于0.99,加标回收率为87%～124%,日内精密度为0.91%～10.31%,日间精密度为4.59%～15.83%,血浆中3种致癌性多环芳烃BaP、B(g,h,i)P、DB(a,h)A的检出限分别为0.33、0.41和0.65μg/L;尿液中3种羟基多环芳烃代谢产物在0.5～100μg/L浓度范围内呈良好的线性关系,线性相关系数均大于0.99,加标回收率为81.8%～110.5%,日内精密度为1.28%～8.56%,日间精密度为6.87%～10.91%,尿液中3种羟基多环芳烃代谢产物2-OHN、2-OHF、1-OHP的检出限分别为0.17、0.03和0.04μg/L。结论该方法生物样本用量少,回收率较高,重现性好,检出限低,适用于人群多环芳烃的生物监测。     

Association of urinary polycyclic aromatic hydrocarbons and serum C-reactive protein

The association of 9 urinary monohydroxy polycyclic aromatic hydrocarbons (OH-PAHs) with serum C-reactive protein (CRP) was investigated using the National Health and Nutrition Examination Survey (NHANES) 2003-2004. The unweighted number of participants included was 999, which represented 139,362,776 persons in the non-institutionalized US population. In adjusted logistic regressions, two OH-PAHs, 2-hydroxyphenanthrene and 9-hydroxyfluorene, were associated with elevated CRP (>3 mg/l). Logistic regressions were adjusted for age, gender, race, exercise, body mass index, smoking status, diabetes, and hypertension. 2-Hydroxyphenanthrene >148 ng/g creatinine had an odds ratio of 3.17 (95% CI 1.73-5.81) compared to 2-hydroxyphenanthrene ≤48 ng/g creatinine, and 9-hydroxyfluorene >749 ng/g creatinine had an odds ratio of 2.28 (95% CI 1.08-4.83) compared to 9-hydroxyfluorene ≤160 ng/g creatinine. Intermediate levels of 2-hydroxyphenanthrene (49-148 ng/g creatinine), and 9-hydroxyfluorene (161-749 ng/g creatinine) were also significantly associated with elevated CRP compared to the respective reference categories.In a combined analysis, OH-PAHs were classified as low, medium, and high. Low OH-PAH was 2-hydroxyphenanthrene ≤48 ng/g creatinine and 9-hydroxyfluorene ≤160 ng/g creatinine. High OH-PAH was 2-hydroxyphenanthrene >148 ng/g creatinine or 9-hydroxyfluorene >749 ng/g creatinine. Participants not assigned to the low or high categories were classified as having medium OH-PAH concentrations. Compared to the low OH-PAH group, high OH-PAH had an odds ratio of 3.60 (95% CI 2.01-6.46) in an adjusted logistic regression. Given that inflammation (characterized here by CRP) is an important factor in the development of atherosclerosis and cardiovascular disease, these results suggest a role for OH-PAHs in the progression of atherosclerosis.     

An examination of the time course from human dietary exposure to polycyclic aromatic hydrocarbons to urinary elimination of 1-hydroxypyrene.

The significance of diet as an exposure route for polycyclic aromatic hydrocarbons (PAHs) and the associated kinetics of urinary 1-hydroxypyrene (1-OHPY) elimination were examined through a controlled human exposure study. Results showed that a 100 to 250-fold increase in a dietary benzo(a)pyrene (BaP) dose paralleled a four to 12-fold increase in urinary 1-OHPy elimination. Mean elimination rates during minimal exposure periods ranged from 6 to 17 ng/h whereas peak elimination rates of 60 to 189 ng/h were seen after a meal high in PAHs. A biexponential model fitted to a limited number of urinary 1-OHPY elimination points gave mean kinetic parameter estimates for t1/2 of 4.4 hours and tmax of 6.3 hours. It is concluded that dietary exposure to PAHs is potentially as substantial as some occupational exposures and therefore requires consideration in studies of exposure to PAHs. The dietary control strategies and the kinetic parameters defined in this investigation provide data for the control of this exposure route when examining other sources of exposure.     

An examination of the time course from human dietary exposure to polycyclic aromatic hydrocarbons to urinary elimination of 1-hydroxypyrene.

The significance of diet as an exposure route for polycyclic aromatic hydrocarbons (PAHs) and the associated kinetics of urinary 1-hydroxypyrene (1-OHPY) elimination were examined through a controlled human exposure study. Results showed that a 100 to 250-fold increase in a dietary benzo(a)pyrene (BaP) dose paralleled a four to 12-fold increase in urinary 1-OHPy elimination. Mean elimination rates during minimal exposure periods ranged from 6 to 17 ng/h whereas peak elimination rates of 60 to 189 ng/h were seen after a meal high in PAHs. A biexponential model fitted to a limited number of urinary 1-OHPY elimination points gave mean kinetic parameter estimates for t1/2 of 4.4 hours and tmax of 6.3 hours. It is concluded that dietary exposure to PAHs is potentially as substantial as some occupational exposures and therefore requires consideration in studies of exposure to PAHs. The dietary control strategies and the kinetic parameters defined in this investigation provide data for the control of this exposure route when examining other sources of exposure.     

Creatinine normalization in biological monitoring revisited: the case of 1-hydroxypyrene

Objectives To compare the apparent urinary excretion rates of both creatinine and 1-hydroxypyrene (1-OHP) and to assess the value of creatinine normalization for both toxicokinetic analysis and the routine examination of workers.Methods All urine samples were collected from individuals who had been exposed to polycyclic aromatic hydrocarbons (PAHs), occupationally and non-occupationally, for at least 24 consecutive hours. Urinary creatinine and 1-OHP were determined. 1-OHP excretion rates were expressed either as a function of creatinine excretion rate or as unadjusted values. Theoretical relationships between creatinine-normalized excretion of metabolites and body weight-adjusted inhaled dose were drawn for men with a constant body mass index.Results Creatinine excretion rate paralleled 1-OHP excretion rate. The plot of creatinine excretion rate–adjusted excretion rate of 1-OHP vs time led to smooth curves for determination of toxicokinetic parameters. Creatinine normalization was adequate, even for samples with a urinary creatinine concentration below 0.5 g/l or above 3 g/l. A theoretical analysis revealed that men weighing between 50 kg and 100 kg, exposed to a constant dose of a pollutant producing a urinary metabolite excreted by the same mechanism as creatinine, would exhibit a body weight-adjusted dose span of 2 with an accompanying creatinine-normalized metabolite excretion span of 2.23-fold.Conclusion The kinetics of creatinine excretion parallels that of 1-OHP, and a creatinine excretion rate–normalized excretion rate of 1-OHP appears to allow for a better determination of the toxicokinetic parameters of 1-OHP urinary excretion. At least in the case of 1-OHP, creatinine normalization seems valid, even for very dilute or very concentrated urine samples. Finally, because creatinine normalization not only compensates for variable diuresis but also correlates better with the body weight-adjusted dose of the parent compound, it should be used in biological monitoring of exposure to (PAHs) pyrene and to other substances whose urinary biomarker excretion kinetics parallel that of creatinine.     

Urinary polycyclic aromatic hydrocarbons as a biomarker of exposure to PAHs in air: a pilot study among pregnant women

Recent studies have linked increased polycyclic aromatic hydrocarbons (PAHs) in air and adverse fetal health outcomes. Urinary PAH metabolites are of interest for exposure assessment if they can predict PAHs in air. We investigated exposure to PAHs by collecting air and urine samples among pregnant women pre-selected as living in "high" (downtown and close to steel mills, n=9) and "low" (suburban, n=10) exposure areas. We analyzed first-morning urine voids from all 3 trimesters of pregnancy for urinary PAH metabolites and compared these to personal air PAH/PM(2.5)/NO(2)/NO(X) samples collected in the 3rd trimester. We also evaluated activities and home characteristics, geographic indicators and outdoor central site PM(2.5)/NO(2)/NO(X) (all trimesters). Personal air exposures to the lighter molecular weight (MW) PAHs were linked to indoor sources (candles and incense), whereas the heavier PAHs were related to outdoor sources. Geometric means of all personal air measurements were higher in the "high" exposure group. We suggest that centrally monitored heavier MW PAHs could be used to predict personal exposures for heavier PAHs only. Urine metabolites were only directly correlated with their parent air PAHs for phenanthrene (Pearson's r=0.31-0.45) and fluorene (r=0.37-0.58). Predictive models suggest that specific metabolites (3-hydroyxyfluorene and 3-hydroxyphenanthrene) may be related to their parent air PAH exposures. The metabolite 2-hydroxynaphthalene was linked to smoking and the metabolite 1-hydroxypyrene was linked to dietary exposures. For researchers interested in predicting exposure to airborne lighter MW PAHs using urinary PAH metabolites, we propose that hydroxyfluorene and hydroxyphenanthrene metabolites be considered.