化妆品中酞酸酯类化合物含量及人群暴露研究

酞酸酯类化合物因具有定香、定型及可增加产品韧性的作用而作为溶剂添加于化妆品中,可通过皮肤、粘膜和呼吸道等途径进入人体。因其对人体有发育和生殖毒性,因此人群经化妆品途径的酞酸酯类化合物的暴露情况需引起关注。本文对化妆品中酞酸酯类化合物含量和经此途径人群暴露研究情况进行综述。     

大气中二噁英的污染现状及健康效应

二噁英是一类持久性有机污染物,也是典型的环境内分泌干扰物,它的毒性极强,可以在环境中持久存在,也能通过食物链富集,因此近年来引起人们的广泛关注。本文概括了二噁英类物质在大气中的污染现状,介绍了人群对于二噁英的呼吸暴露风险,总结了人体接触二噁英后可能产生的健康效应,并对今后的控制工作提出了建议。在二噁英浓度较高的城市及其功能区,长期吸入污染物对人群的健康和寿命具有潜在风险。建议对垃圾进行有序分类,追踪并监测垃圾焚烧厂周围居民的健康状况,并建立相关排放标准及限值,对二噁英的排放逐渐规范化、无害化。     

2,3,7,8-四氯二苯并二噁英所致皮肤损害的研究进展

2,3,7,8-四氯二苯并二噁英（2,3,7,8-tetrachlorodibenzop-dioxin,TCDD）是二噁英类化合物中毒性最强的一种,是WHO列出的12类最严重的持续性环境有机污染物之一.TCDD具有亲脂性，体内半衰期长达5，8年，不易排除；对皮肤、免疫系统、生殖系统、消化系统及内分泌系统等都有毒害作用，其中，氯痤疮及与之相关的皮肤及附属器的病变是人类暴露于TCDD后出现的最敏感、最广泛的症状之一。     

垃圾焚烧发电地区儿童二噁英暴露水平及特征研究

目的分析垃圾焚烧发电厂周边儿童体内二噁英负荷水平、分布特征和人群二噁英外暴露水平。方法设距垃圾焚烧发电厂1km S镇为污染点,200km外的L镇为对照点,采集S镇90名及L镇60名10～11岁儿童外周静脉血,另采集两地土壤、鲫鱼和鸡蛋各3份,检测样本中二噁英浓度及计算毒性当量(TEQ)并分析对比。结果污染点儿童血中二噁英浓度与TEQ均显著高于对照组(P<0.05);鸡蛋和鲫鱼中二噁英浓度与TEQ、土壤中二噁英浓度均显著高于对照组(P<0.05)。两地样本的二噁英单体分布类似,其中单体浓度最高的为八氯代二苯并二噁英(OCDD),TEQ贡献最高的为2,3,4,7,8-五氯代二苯并呋喃(2,3,4,7,8-PeCDF)。结论垃圾焚烧发电厂周边土壤中二噁英浓度增高,当地儿童噁恶英外暴露和内负荷水平均显著增高。     

环境雌激素暴露与糖尿病发病关系研究进展

近年来,糖尿病、肥胖等慢性代谢性疾病成为公共卫生领域研究热点,环境雌激素(EEs)暴露成为继基因、行为及生活方式等导致糖尿病又一危险因素;各类EEs化学结构不同,因此长期暴露后诱发糖尿病的机制也不相同;双酚A(BPA)和二噁英(TCDD)是研究较多的具有胰岛素分泌干扰活性的EEs化合物,近年来发现壬基酚(NP)的高胰岛素效应也是不可忽视的,为此本文综述了几种主要的EEs暴露与糖尿病发病可能潜在的作用机理及面临的问题,为预防糖尿病和控制糖尿病发病率提出建议。     

废水中二噁英类化合物测定的固相微萃取前处理法

目的探讨废水中二噁英类化合物测定的固相微萃取处理法.方法采用固相微萃取(SPME)装置对样品进行纯化和富集,以HRGC-HRMS分析废水中的二噁英类化合物.结果最佳萃取温度和时间分别为45℃、30 main.检测限为0.05 pg/μl,相对标准偏差＜10%,回收率为99%～102%,样品中二噁英类物质总的浓度为0.78 pg/μl.结论用SPME方法测定废水中的二噁英类化合物,操作简便快速,有广阔的应用前景.     

过量锰、铁、铝暴露对胰岛细胞及糖尿病影响的研究

目的 总结过量锰、铁、铝暴露对胰岛细胞及糖尿病影响的研究进展。方法 通过用“锰”、“铁”、“铝”、“胰岛细胞”、“糖尿病”等关键字或主题,在PubMed、SpringerLink、CNKI、万方数据库进行文献检索,筛选国内外文献53篇,其中近5年文献占49%。结果 过量锰、铁、铝单独暴露可在大鼠胰腺蓄积,引起β细胞受损和体内糖代谢障碍,染毒途径、剂量、期限不同对胰腺损伤程度不一。过量锰或铁暴露可能与人群血糖升高或糖尿病发病有关,过量铝暴露使患糖尿病、胰腺癌风险增高。结论 过量单独锰、铁和铝实验性暴露可以对胰岛细胞及糖尿病产生明显的影响,其严重程度受到染毒途径、剂量、时间不同的影响。环境或职业性铝人群暴露可能是糖尿病发生的重要影响因素之一,过量锰、铁暴露对人群胰岛细胞及糖尿病的影响尚缺乏足够证据。     

北京某垃圾焚烧厂二噁英多介质扩散风险评估

目的基于北京某垃圾焚烧厂的二噁英排放数据,评估其周边居民通过不同暴露途径面临的健康风险。方法参考美国加州热点计划,采用AERMOD模型,模拟北京某垃圾焚烧厂排放二噁英在大气中的扩散情况;借助多介质扩散模型,模拟二噁英在不同环境介质中的扩散情况;计算垃圾焚烧厂周边居民通过不同暴露途径的二噁英摄入量,评估人群终身致癌风险。结果在垃圾焚烧厂周边最大落地点浓度处,居民通过呼吸、皮肤接触、泥土摄入和母乳喂养等途径面临的终身致癌风险为5.28×10~(-7);当居民饮用水来自于5大水库,饮食取自垃圾焚烧厂周边蔬菜基地、养殖场和水库时,所面临的终身致癌风险为1.77×10~(-8)。结论该垃圾焚烧厂在现有排放状况下,其周边居民面临的健康风险在充分安全边际内,其中呼吸和母乳喂养是最主要的暴露途径。     

2007年北京市居民母乳中二噁英类化合物负荷水平调查

目的 调查北京地区居民母乳中多氯代苯并二噁英和多氯代苯并呋喃(PCDD/Fs)和二噁英样多氯联苯(dl-PCBs)的污染水平,评价一般人群PCDD/Fs和dl-PCBs的机体负荷状况.方法 2007年在北京市11个区、县中采集母乳样品110份,制成11个混合样品后,采用同位素稀释技术以高分辨气相色谱-高分辨质谱(HRGC-HRMS)测定母乳样品中的PCDD/Fs和dl-PCBs.结果 北京市母乳样品中二噁英类化合物含量最高的组分为八氯代二苯并二噁英(OCDD)和多氯联苯(PCB)-118、PCB-105,其含量中位数分别为20.6 pg/g脂肪、4.07和1.63 ng/g脂肪.按毒性当量(TEQ)计,北京市11个母乳混合样品中总二噁英类化合物含量中位数为7.4 pg TEQ/g脂肪;最高的为通州区,含量中位数为13.5 pg TEQ/g脂肪;最低的为平谷区,为4.3 pg TEQ/g脂肪.结论 目前北京市母乳中PCDD/Fs和dl-PCBs处于较低水平,但随着我国的快速工业化,人群此类物质的机体负荷水平有可能会上升,因此有必要持续跟踪监测.     

我国普通人群二(口恶)英类化合物暴露风险评估

该文对世界工业发达国家普通人群体内二(口恶)英类化合物(PCDD/Fs、PCBs)水平和变化趋势及饮食暴露状况进行了综述.根据我国现有人体中PCDD/Fs含量实测数据,对我国人体中PCDD/Fs、PCBs水平进行评价和对比.研究认为我国普通人群人体中二(口恶)英类化合物水平与工业发达国家相比处于较低水平.此外,估算了我国普通人群日常饮食的暴露水平,认为我国普通人群日常饮食暴露水平低于世界卫生组织(WHO)专家建议的每日容许摄入量,处于安全水平线内.     

Dioxin emissions from a solid waste incinerator and risk of non-Hodgkin lymphoma

BACKGROUND: It is not clear whether low environmental doses of dioxin affect the general population. We previously detected a cluster of patients with non-Hodgkin lymphoma around a French municipal solid waste incinerator with high dioxin emissions. To explore the environmental route suggested by these findings, we carried out a population-based case-control study in the same area. METHODS: We compared 222 incident cases of non-Hodgkin lymphoma diagnosed between 1980 and 1995 and controls randomly selected from the 1990 population census, using a 10-to-1 match. Dioxin ground-level concentrations were modeled with a second-generation Gaussian-type dispersion model, yielding four dioxin exposure categories. The latter were linked to individual places of residence, using Geographic Information System technology. RESULTS: The risk of developing non-Hodgkin lymphoma was 2.3 times higher (95% confidence interval = 1.4-3.8) among individuals living in the area with the highest dioxin concentration than among those living in the area with the lowest dioxin concentration. No increased risk was found for the intermediate dioxin exposure categories. Adjustment for a wide range of socioeconomic characteristics at the block group level did not alter the results. CONCLUSION: Although emissions from incinerators are usually not regarded as an important source of exposure to dioxins compared with other background sources, our findings support the hypothesis that environmental dioxins increase the risk of non-Hodgkin lymphoma among the population living in the vicinity of a municipal solid waste incinerator.     

Sarcoma risk and dioxin emissions from incinerators and industrial plants: a population-based case-control study (Italy)

Background  

It is not clear whether environmental exposure to dioxin affects the general population. The aim of this research is to evaluate sarcoma risk in relation to the environmental pollution caused by dioxin emitted by waste incinerators and industrial sources of airborne dioxin. The study population lives in a part of the Province of Venice (Italy), where a population-based cancer registry (Veneto Tumour Registry – RTV) has been active since 1987.     

Short- and long-term morbidity and mortality in the population exposed to dioxin after the "Seveso accident"

The early effects of 2,3,7,8-tetrachlorodibenzo-para-dioxin (TCDD) exposure in the population involved in the Seveso, Italy, incident in 1976, have been examined in numerous studies. Chloracne was the only effect linked with sufficient certainty to dioxin exposure. The possible long-term consequences were investigated with mortality and cancer incidence studies. Mortality and morbidity findings during the 20-year period following the accident showed increased risk from lymphoemopoietic neoplasm, digestive system cancer (rectum in males, and biliary tract among females, in particular) and respiratory system cancer (lung, among males). In the incidence analyses, also thyroid gland and pleura cancer appeared suggestively increased. Soft tissue sarcomas showed an increase in the largest, yet least exposed, exposure sub-cohort. Several hypotheses associating non-cancer effects with dioxin exposure were corroborated by findings in the Seveso population: this was the case with cardiovascular effects (possibly linked to both chemical exposure and stressful disaster experience), endocrine effects (diabetes among females) and reproductive effects: exposure of men to TCDD was linked to a lowered male/female sex ratio in their offspring. The results of many Seveso studies point to possible gender effects, in accordance with animal models. Notwithstanding the acknowledged study limitations (lack of individual exposure markers, short latency, and small population size for certain cancer types), results of previous experimental and epidemiological studies, along with mechanistic knowledge on dioxin toxicity, support the hypotheses that the observed excesses might be associated with dioxin exposure. The mortality and cancer incidence follow-up of the Seveso cohort are continuing.     

Dioxin: exposure-response analyses and risk assessment

Low-levels of dioxin cause cancer in animals. In 1997 dioxin was found to be a human carcinogen by the International Agency for Research on Cancer, based largely on four studies of industrial workers exposed to high levels. Recently there has been interest in estimating human cancer risk at low level environmental exposures. Here we review quantitative exposure-response analyses and risk assessment for low environmental levels based on the largest existing cohort of workers exposed to dioxin (the U.S. NIOSH cohort). We estimate that doubling background levels of exposure, which may occur for example by eating a lot of fish which have accumulated dioxin, will increase lifetime risk of cancer death by 0.1 to 1.0%. In the US the background risk of cancer death by age 75 is 12%, so doubling background levels of dioxin exposure would increase this lifetime risk to somewhere between 12.1 and 13.0%. Our results agree broadly with results from a German cohort, which is the only other cohort for which a quantitative risk assessment has been conducted.     

Serum dioxin level in relation to diabetes mellitus among Air Force veterans with background levels of exposure

Data from several epidemiologic studies suggest that exposure to unusually high amounts of dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin) increases the risk of diabetes mellitus, and experimental data suggest that the mechanism for this is decreased cellular glucose uptake. To investigate the dose-response relation more closely, we examined the association of serum dioxin level with prevalence of diabetes mellitus and with levels of serum insulin and glucose among 1,197 veterans in the Air Force Health Study who never had contact with dioxin-contaminated herbicides and whose serum dioxin level was within the range of background exposure typically seen in the United States (< or =10 ng/kg lipid). Compared with those whose serum dioxin level was in the first quartile (<2.8 ng/kg lipid), the multivariate-adjusted odds of diabetes among those in the highest quartile (> or =5.2 ng/kg lipid) was 1.71 (95% confidence interval = 1.00-2.91). The association was slightly attenuated after adjustment for serum triglycerides. Whether adjustment for serum triglycerides was appropriate, however, cannot be determined with available data. The association of background-level dioxin exposure with the prevalence of diabetes in these data may well be due to reasons other than causality, although a causal contribution cannot be wholly dismissed.     

Environmental contaminants as risk factors for developing diabetes

The contribution of exposure to persistent organic pollutants (POPs) to the incidence of diabetes has received little attention until recently. A number of reports have emerged, however, concerning elevated diabetes in persons occupationally exposed to dioxin. United States (US) Air Force personnel in Vietnam who sprayed Agent Orange containing dioxin as a contaminant had elevated rates of diabetes, leading to US government compensation for diabetes in these veterans. Recent studies in populations exposed to polychlorinated biphenyls (PCBs) and chlorinated pesticides found a dose-dependent elevated risk of diabetes. An elevation in risk of diabetes in relation to levels of several POPs has been demonstrated by two different groups using the National Health and Nutrition Examination Survey (NHANES), a random sampling of US citizens. The strong associations seen in quite different studies suggest the possibility that exposure to POPs could cause diabetes. One striking observation is that obese persons that do not have elevated POPs are not at elevated risk of diabetes, suggesting that the POPs rather than the obesity per se is responsible for the association. Although a specific mechanism is not known, most POPs induce a great number and variety of genes, including several that alter insulin action. Because diabetes is a dangerous disease that is increasing in frequency throughout the world, further study of the possibility that exposure to POPs contributes to the etiology of diabetes is critical.     

Possible risk of endometriosis for Seveso, Italy, residents: an assessment of exposure to dioxin.

A recent study by Rier et al. showed that rhesus monkeys exposed daily for 4 years to 5 or 25 ppt of dioxin in food develop endometriosis, with incidence and severity related to dose. We aimed to determine whether the total time-integrated dioxin exposure of a human population could be comparable to that of Rier's monkeys. We selected a sample of residents of Seveso, Italy, who were acutely exposed to high levels of dioxin following an accident in 1976. We conducted a toxicokinetic analysis which takes into account species and exposure differences in dose and timing between humans and monkeys. The area under the time-concentration curve for dioxin in fat, which corresponds to cumulative exposure over time, ranges for some of the most heavily exposed Seveso residents from approximately 1.7 x 10(6) ppt-days to 1.1 x 10(8) ppt-days. These values exceed in all cases the values for the monkeys exposed to 25 ppt or 5 ppt. Given their exposure, the Seveso population should be an ideal epidemiologic cohort to rule out or confirm whether exposure to dioxin leads to an increased risk of endometriosis in humans.     

Elimination Rates of Dioxin Congeners in Former Chlorophenol Workers from Midland,Michigan

Background: Exposure reconstructions and risk assessments for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and other dioxins rely on estimates of elimination rates. Limited data are available on elimination rates for congeners other than TCDD.Objectives: We estimated apparent elimination rates using a simple first-order one-compartment model for selected dioxin congeners based on repeated blood sampling in a previously studied population.Methods: Blood samples collected from 56 former chlorophenol workers in 2004–2005 and again in 2010 were analyzed for dioxin congeners. We calculated the apparent elimination half-life in each individual for each dioxin congener and examined factors potentially influencing elimination rates and the impact of estimated ongoing background exposures on rate estimates.Results: Mean concentrations of all dioxin congeners in the sampled participants declined between sampling times. Median apparent half-lives of elimination based on changes in estimated mass in the body were generally consistent with previous estimates and ranged from 6.8 years (1,2,3,7,8,9-hexachlorodibenzo-p-dioxin) to 11.6 years (pentachlorodibenzo-p-dioxin), with a composite half-life of 9.3 years for TCDD toxic equivalents. None of the factors examined, including age, smoking status, body mass index or change in body mass index, initial measured concentration, or chloracne diagnosis, was consistently associated with the estimated elimination rates in this population. Inclusion of plausible estimates of ongoing background exposures decreased apparent half-lives by approximately 10%. Available concentration-dependent toxicokinetic models for TCDD underpredicted observed elimination rates for concentrations < 100 ppt.Conclusions: The estimated elimination rates from this relatively large serial sampling study can inform occupational and environmental exposure and serum evaluations for dioxin compounds.     

Attenuation of exposure-response curves in occupational cohort studies at high exposure levels

Numerous occupational cohort mortality studies have observed exposure-response curves to have an increasing slope at low exposure levels that attenuates or even turns negative at high exposure levels. Examples discussed in this paper include dioxin, silica, 1,3-butadiene, cadmium, beryllium, radon daughters, diesel fumes, nickel, arsenic, and hexavalent chromium. Possible explanations for this phenomenon include (i) bias introduced by the healthy worker survivor effect, (ii) a depletion of the number of susceptible people in the population at high exposure levels, (iii) a natural limit on the relative risk for diseases with a high background rate, (iv) mismeasurement or misclassification of exposures, (v) the influence of other risk factors that vary by the level of the main exposure, and (vi) the saturation of key enzyme systems or other processes involved in the development of disease.