Study Of Human Internal Exposure To Typical Organic Pollutants And Health Effects

Organic pollutants are a group of ubiquitous chemicals with lipophilicity and potential adversehealth effects on reproductive and endocrine systems. The accurate assessment of exposure levelsand the health effects are the theoretical basis to control those pollutants. Compared with externalenvironmental exposure concentrations, internal dose of organic pollutants were the biomarkers ofthe total dose which have been entered into the human body via kinds of exposure routes. Thus,internal concentrations are the key to link environmental exposure to health effects. In this thesis,analytical methods of exposure biomarkers were set up. Two population studies were investigatedbased on internal exposure methods:1) characteristics of human exposure to organic pollutants in atypical contaminant environment (an electronic waste dismantling area), and the subsequent healtheffects;2) screening typical organic pollutants which could increase the risk of polycystic ovarysyndrome (PCOS), one of the typical outcomes of endocrine disorders. The aim of this study was toexplore the dose-response relationship between pollutants and health effects.High sensitive and selective analytical methods with GC-MS-EI/ECNI were developed todetermine the pollutants in blood (serum or plasma) and urinary samples. Internal levels of organicpollutants and the metabolites, including PBDEs, PCBs, PBB153, DP, PAHs/HO-PAHs and typicalEDCs, could be measured.In the e-waste dismantling exposure research, the study population (including e-waste workersand local residents) were from an e-waste area in Northern China. People living40km away werechosen as the control group. The results indicated that serum concentrations of PBDE4-6, PBDE7-9,PCBs, PBB153and DP in the exposure population group were2.5(95%CI:1.5-4.2),1.8(1.3-2.4),4.3(3.0-6.3),8.7(5.3-14.4) and5.8(3.6-9.5)-fold higher than those in the control group. Therelatively high exposure to tetra-to nona-BDE and PBB153combined with vacant records ofproduction and consumption indicated that e-waste from abroad was the major exposure source ofthese pollutants to the population in the dismantling region. The resident site and occupationalexposurethroughthe e-waste dismantling process werethe twosignificantimpact factors ofinternalexposure to BPAand mEHP, respectively. mEHPwas the exposure biomarker to PAEs. The urinaryconcentrations of BPA in the exposure area were2.4(1.3-4.5)-fold higher than those of controlpopulation; while levels of urinary mEHP in the e-waste dismantling workers were4.7(1.6-13.5)-fold higherthanthoseofother non-occupationalexposurepopulation. Inthis typicalruralpopulationin North China, high levels of urinary hydroxy-PAHs were observed. Particularly in the winterseason, the exposures were2.3-6.0-fold of those in the spring. The dose-response relationshipsbetween pollutants and lipid peroxidation, DNA oxidative damage were observed. Serum levels ofMDA significantly positively correlated with PBDEs, PBB153and DP. The estimations indicated21.3%-39.3%increment of urinary MDA per one-fold increase of hydroxy-PAHs, while16.1%(6.8%-26.1%)and13.1%(4.7%-22.3%)incrementper one-foldincrease ofurinaryBPAand mEHP,respectively. Moreover, significant correlation was found between urinary8-OHdG and BPA,indicating that59.9%(36.3%-87.5%) increment of8-OHdG with one-fold increasing of internal exposure to BPA. These results provide evidences on high typical organic pollutants exposure andtheinduction of oxidativestress onlipid peroxidationand DNAoxidativedamageinthis population.The population in PCOS case-control study consisted of50cases and30healthy femalecontrols. The results showed that serum levels of PAHs, NP, p,p’-DDE and PCBs in the case groupwere significantly higher than levels of the control. These typical organic pollutants significantlyshowedassociations withthePCOSrisk. After considering effects ofconfoundingfactors, includingage, total cholesterol, triglycerides, the ORs of PAHs, p,p’-DDE and dl-PCBs were3.61(95%CI:1.26-10.4)、3.38(1.18-9.62)and4.69(1.51-14.6).Lineardose-responserelationshipswereobservedbetweenPAHs, p,p’-DDEandPCBs andrisk ofPCOS. Instratifiedanalysis, BMIshoweda positiveconfounding effect to the relationship between PAHs and the risk of PCOS. However, the levels ofPCBs and ORs of PCBs in the population with BMI <25kg m-2were significantly higher. Thepositiveconfoundingeffects ofinsulinresistancewereobservedtoseveralkinds ofPCBscongeners.In all, the significant associations betweenincreased risk of PCOS and high internal exposure levelsof PAHs, p,p’-DDE and PCBs were found after the stratified analysis. Elevated levels of BMI, lipid,LH, androgen and insulin in PCOS group were found. Moreover, the concentrations of pollutantsalso showed positively correlated with those indicators, including FSH and glucose. Those resultsindicated that organic pollutants may increase risk of PCOS, possibly through lipid metabolism,hormone, synthesis and secretion of insulin and glucose metabolism to disrupt the whole endocrinesystem. This investigation systematically reported over50kinds of environmental risks to PCOSbased on the internal exposure to organic pollutants. Based on the multivariate data analysis, thepotential adverse health effects and risks of PCOS from environmental pollutants were of greatimportance, possibly greater than other risk factors.