Persistent organic pollutants and the incidence of type 2 diabetes in the CARLA and KORA cohort studies.

BACKGROUND: Associations between several persistent organic pollutants (POPs) and type 2 diabetes have been found in humans, but the relationship has rarely been investigated in the general population. The current nested case-control study examined internal exposure to polychlorinated biphenyls (PCB) and pesticides and the incidence of type 2 diabetes among participants of two population-based German cohort studies. METHODS: We retrospectively selected 132 incident cases of type 2 diabetes and 264 age- and sex-matched controls from the CARdiovascular Living and Aging in Halle (CARLA) study (2002-2006, East Germany) and the Cooperative Health Research in the Region of Augsburg (KORA) study (1999-2001, South Germany) based on diabetes status at follow-up examinations in 2007-2010 and 2006-08, respectively (60% male, mean age 63 and 54 years). We assessed the association between baseline POP concentrations and incident diabetes by conditional logistic regression adjusted for cohort, BMI, cholesterol, alcohol, smoking, physical activity, and parental diabetes. Additionally, we examined effect modification by sex, obesity, parental diabetes and cohort. RESULTS: In both cohorts, diabetes cases showed a higher BMI, a higher frequency of parental diabetes, and higher levels of POPs. We observed an increased chance for incident diabetes for PCB-138 and PCB-153 with an odds ratio (OR) of 1.50 (95%CI: 1.07-2.11) and 1.53 (1.15-2.04) per interquartile range increase in the respective POP. In addition, explorative results suggested higher OR for women and non-obese participants. CONCLUSIONS: Our results add to the evidence on diabetogenic effects of POPs in the general population, and warrant both policies to prevent human exposure to POPs and additional research on the adverse effects of more complex chemical mixtures.

Human biomonitoring pilot study DEMOCOPHES in Germany: Contribution to a harmonized European approach.

Human biomonitoring (HBM) is an effective tool to assess human exposure to environmental pollutants, but comparable HBM data in Europe are lacking. In order to expedite harmonization of HBM studies on a European scale, the twin projects COPHES (Consortium to Perform Human Biomonitoring on a European Scale) and DEMOCOPHES (Demonstration of a study to Coordinate and Perform Human Biomonitoring on a European Scale) were formed, comprising 35 partners from 27 European countries. In COPHES a research scheme and guidelines were developed to exemplarily measure in a pilot study mercury in hair, cadmium, cotinine and several phthalate metabolites in urine of 6-11year old children and their mothers in an urban and a rural region. Seventeen European countries simultaneously conducted this cross-sectional DEMOCOPHES feasibility study. The German study population was taken in the city of Bochum and in the Higher Sauerland District, comprising 120 mother-child pairs. In the present paper features of the study implementation are presented. German exposure concentrations of the pollutants are reported and compared with European average concentrations from DEMOCOPHES and with those measured in the representative German Environmental Survey (GerES IV). German DEMOCOPHES concentrations for mercury and cotinine were lower than the European average. However, 47% of the children were still exposed to environmental tobacco smoke (ETS) outside their home, which gives further potential for enhancing protection of children from ETS. Compared with samples from the other European countries German participating children had lower concentrations of the phthalate metabolites MEP and of the sum of 3 DEHP-metabolites (MEHP, 5OH-MEHP and 5oxo-MEHP), about the same concentrations of the phthalate metabolites MBzP and MiBP and higher concentrations of the phthalate metabolite MnBP. 2.5% of the German children had concentrations of the sum of 4 DEHP-metabolites and 4.2% had concentrations of MnBP that exceeded health based guidance values, indicating reasons for concern. Continuous HBM is necessary to track changes of pollutant exposure over time. Therefore Germany will continue to cooperate on the harmonisation of European human biomonitoring to support the chemicals regulation with the best possible exposure data to protect Europe's people against environmental health risks.

Prenatal exposure to PCB-153, p,p'-DDE and birth outcomes in 9000 mother-child pairs: exposure-response relationship and effect modifiers.

Low-level exposure to polychlorinated biphenyl-153 (PCB-153) and dichlorodiphenyldichloroethylene (p-p'-DDE) can impair fetal growth; however, the exposure-response relationship and effect modifiers of such association are not well established. This study is an extension of an earlier European meta-analysis. Our aim was to explore exposure-response relationship between PCB-153 and p-p'-DDE and birth outcomes; to evaluate whether any no exposure-effect level and susceptible subgroups exist; and to assess the role of maternal gestational weight gain (GWG). We used a pooled dataset of 9377 mother-child pairs enrolled in 14 study populations from 11 European birth cohorts. General additive models were used to evaluate the shape of the relationships between organochlorine compounds and birth outcomes. We observed an inverse linear exposure-response relationship between prenatal exposure to PCB-153 and birth weight [decline of 194g (95% CI -314, -74) per 1µg/L increase in PCB-153]. We showed effects on birth weight over the entire exposure range, including at low levels. This reduction seems to be stronger among children of mothers who were non-Caucasian or had smoked during pregnancy. The most susceptible subgroup was girls whose mothers smoked during pregnancy. After adjusting for absolute GWG or estimated fat mass, a reduction in birth weight was still observed. This study suggests that the association between low-level exposure to PCB-153 and birth weight exists and follows an inverse linear exposure-response relationship with effects even at low levels, and that maternal smoking and ethnicity modify this association.

Determination of polychlorinated biphenyls and organochlorine pesticides in small volumes of human blood by high-throughput on-line SPE-LVI-GC-HRMS.

A fully automated and robust method featuring on-line solid-phase extraction (SPE) and large volume injection (LVI) gas chromatographic (GC) high resolution mass spectrometry (HRMS) is used to determine polychlorinated biphenyls (PCBs) and organochlorine pesticides, such as penta- and hexachlorobenzene (PeCBz, HxCBz), hexachlorocyclohexane isomers (HCH) and 4,4'-dichlorodiphenyldichloroethene (a metabolite of dichlorodiphenyltrichloroethane (DDT)), with only 200µl of human blood, serum or plasma. After spiking the sample with (13)C-labeled internal standards and precipitating the proteins, the sample is passed through a 10mm×2.0mm ID SPE cartridge filled with C18 material that adsorbs the analytes. After washing and drying, the cartridge is extracted with hexane/dodecane (99/1, v/v); the extract is directly injected into a LVI where GC/HRMS analysis follows. The fully automated system utilizes a robotic autosampler and a modular SPE system including two high-pressure syringe pumps, an automatic SPE cartridge exchanger unit and 6 switchable valves. All sample preparation steps are performed within 20min during the GC run of a previous sample, limiting the throughput with only the GC runtime. The contents are quantified using the isotope dilution method. Due to laboratory air contamination problems, we achieved LOQs of 0.017 (PeCBz), 0.009 (HxCBz), 0.007 (HCH), 0.016 (DDE), while for the six indicator PCBs, we achieved values of 0.030 (PCB-28), 0.044 (PCB-52), 0.024 (PCB-101), 0.009 (PCB-138), 0.015 (PCB-153) and 0.008 (PCB-180)µg/l serum. Under clean laboratory air conditions, these values may be improved. This method is recommended when high throughput is desirable and/or only small amounts of material are available, such as during studies involving children.

High levels of PAH-metabolites in urine of e-waste recycling workers from Agbogbloshie, Ghana.

The informal recycling of electronic waste (e-waste) is an emerging source of environmental pollution in Africa. Among other toxins, polycyclic aromatic hydrocarbons (PAHs) are a major health concern for exposed individuals. In a cross-sectional study, the levels of PAH metabolites in the urine of individuals working on one of the largest e-waste recycling sites of Africa, and in controls from a suburb of Accra without direct exposure to e-waste recycling activities, were investigated. Socioeconomic data, basic health data and urine samples were collected from 72 exposed individuals and 40 controls. In the urine samples, concentrations of the hydroxylate PAH metabolites (OH-PAH) 1-hydroxyphenanthrene (1-OH-phenanthrene), the sum of 2- and 9-hydroxyphenanthrene (2-/9-OH-phenanthrene), 3-hydroxyphenanthrene (3-OH-phenanthrene), 4-hydroxyphenanthrene (4-OH-phenanthrene) and 1-hydroxypyrene (1-OH-pyrene), as well as cotinine and creatinine, were determined. In the exposed group, median urinary concentrations were 0.85 µg/g creatinine for 1-OH-phenanthrene, 0.54 µg/g creatinine for 2-/9-OH-phenanthrene, 0.99 µg/g creatinine for 3-OH-phenanthrene, 0.22 µg/g creatinine for 4-OH-phenanthrene, and 1.33 µg/g creatinine for 1-OH-pyrene, all being significantly higher compared to the control group (0.55, 0.37, 0.63, 0.11 and 0.54 µg/g creatinine, respectively). Using a multivariate linear regression analysis including sex, cotinine and tobacco smoking as covariates, exposure to e-waste recycling activities was the most important determinant for PAH exposure. On physical examination, pathological findings were rare, but about two thirds of exposed individuals complained about cough, and one quarter about chest pain. In conclusion, we observed significantly higher urinary PAH metabolite concentrations in individuals who were exposed to e-waste recycling compared to controls who were not exposed to e-waste recycling activities. The impact of e-waste recycling on exposure to environmental toxins and health of individuals living in the surroundings of e-waste recycling sites warrant further investigation.

Levels and predictors of urinary nickel concentrations of children in Germany: results from the German Environmental Survey on children (GerES IV).

Human biomonitoring of nickel has gained interest in environmental medicine due to its wide distribution in the environment and its allergenic potential. There are indications that the prevalence of nickel sensitization in children is increased by nickel exposure and that oral uptake of nickel can exacerbate nickel dermatitis in nickel-sensitive individuals. Urinary nickel measurement is a good indicator of exposure. However, data on nickel levels in urine of children are rare. For the first time, the German Environmental Survey on children (GerES IV) 2003-2006 provided representative data to describe the internal nickel exposure of children aged 3-14 years in Germany. Nickel was measured after enrichment in the organic phase of urine by graphite furnace atomic absorption spectrometry with Zeeman background correction. Nickel levels (n=1576) ranged from <0.5 to 15 µg/l. Geometric mean was 1.26 µg/l. Multivariate regression analysis showed that gender, age, socio-economic status, being overweighted, consumption of hazelnut spread, nuts, cereals, chocolate and urinary creatinine were significant predictors for urinary nickel excretion of children who do not smoke. 20.2% of the variance could be explained by these variables. With a contribution of 13.8% the urinary creatinine concentration was the most important predictor. No influence of nickel intake via drinking water and second hand smoke exposure was observed.

Determination of bisphenol a in urine from mother-child pairs-results from the duisburg birth cohort study, Germany.

Bisphenol A (BPA) may alter endocrine functions, and human exposure is widespread. In the Duisburg birth cohort study the influence of several contaminants was examined on the neuropsychological and pubertal development of children. This study reports the biomonitoring results on BPA within the 6-yr follow-up study (children's age 6-8 yr). Total BPA and free (unconjugated) BPA concentrations in 208 urine samples of 104 mother-child pairs were measured. For quality control, total BPA was analyzed by two independent laboratories. BPA was detected in all urine samples, while free BPA was observed above the limit of quantification (LOQ) in only 33 samples. Total BPA concentrations were significantly associated between the two laboratories. BPA concentrations (median; range) tended to be higher in children than in mothers but the difference was not significant. Total BPA levels in children and mothers correlated at low levels but significantly to each other. Multivariate linear regression analysis revealed positive associations between creatinine and the BPA concentrations and a negative association with German nationality (mothers only). Evidence indicates that BPA exposure is omnipresent but levels in mother-child pairs are low. Only small amounts (less than 16%) were detectable as free (unconjugated) BPA. Analytical reliability is high even at such low levels, provided that external contamination is minimized.

Birth weight and prenatal exposure to polychlorinated biphenyls (PCBs) and dichlorodiphenyldichloroethylene (DDE): a meta-analysis within 12 European Birth Cohorts.

OBJECTIVES: Exposure to high concentrations of persistent organochlorines may cause fetal toxicity, but the evidence at low exposure levels is limited. Large studies with substantial exposure contrasts and appropriate exposure assessment are warranted. Within the framework of the EU (European Union) ENRIECO (ENvironmental Health RIsks in European Birth Cohorts) and EU OBELIX (OBesogenic Endocrine disrupting chemicals: LInking prenatal eXposure to the development of obesity later in life) projects, we examined the hypothesis that the combination of polychlorinated biphenyls (PCBs) and dichlorodiphenyldichloroethylene (DDE) adversely affects birth weight. METHODS: We used maternal and cord blood and breast milk samples of 7,990 women enrolled in 15 study populations from 12 European birth cohorts from 1990 through 2008. Using identical variable definitions, we performed for each cohort linear regression of birth weight on estimates of cord serum concentration of PCB-153 and p,p´-DDE adjusted for gestational age and a priori selected covariates. We obtained summary estimates by meta-analysis and performed analyses of interactions. RESULTS: The median concentration of cord serum PCB-153 was 140 ng/L (range of cohort medians 20-484 ng/L) and that of p,p´-DDE was 528 ng/L (range of cohort medians 50-1,208 ng/L). Birth weight decreased with increasing cord serum concentration of PCB-153 after adjustment for potential confounders in 12 of 15 study populations. The meta-analysis including all cohorts indicated a birth weight decline of 150 g [95% confidence interval (CI): -250, -50 g] per 1-µg/L increase in PCB-153, an exposure contrast that is close to the range of exposures across the cohorts. A 1-µg/L increase in p,p´-DDE was associated with a 7-g decrease in birth weight (95% CI: -18, 4 g). CONCLUSIONS: The findings suggest that low-level exposure to PCB (or correlated exposures) impairs fetal growth, but that exposure to p,p´-DDE does not. The study adds to mounting evidence that low-level exposure to PCBs is inversely associated with fetal growth.

Prevalence of nickel sensitization and urinary nickel content of children are increased by nickel in ambient air.

In a cross-sectional study performed in 2000, an unexpected positive association between nickel (Ni) in ambient air, urinary Ni content and the prevalence of Ni sensitization in a subgroup of 6-yr-old children living near a steel mill was observed. Between 2005 and 2006, in a different and larger study population, we examined if Ni from ambient air or urinary Ni concentration was related to Ni sensitization in children living next to Ni-emitting steel mills. We studied 749 school beginners living in four Ni-polluted industrial areas of North Rhine-Westphalia, Germany. We assessed Ni in ambient air, Ni in urine from children and mothers, and Ni in tap water, conducted patch tests in children (including the NiSO(4)-dilution test) and collected questionnaire data. Statistics were done by linear and logistic regression analyses, adjusted for covariates. At increased Ni concentration in ambient air (unit of increase: 10 ng/m(3)), urinary Ni concentrations rose in both mothers (9.1%; 95% CI: 6.8-11.4%) and children (2.4%; 95% CI: 0.4-4.4%). The prevalence of Ni sensitization in children was associated with increased Ni from ambient air (unit of increase: 18 ng/m(3); odds ratio 1.28; 95% CI: 1.25-1.32) and urinary Ni concentration (unit of increase: 7.1 µg/L; odds ratio 2.4; 95% CI: 1.20-4.48). Ni in ambient air of areas with Ni-emitting factories contributes to internal Ni exposure in residents via inhalation and, furthermore, is a risk factor for the development of Ni sensitization in children.

Does airborne nickel exposure induce nickel sensitization?

BACKGROUND AND OBJECTIVE: Nickel is one of the most prevalent causes of contact allergy in the general population. This study focuses on human exposure to airborne nickel and its potential to induce allergic sensitization. MATERIALS AND METHODS: The study group consisted of 309 children at school-starter age living in the West of Germany in the vicinity of two industrial sources and in a rural town without nearby point sources of nickel. An exposure assessment of nickel in ambient air was available for children in the Ruhr district using routinely monitored ambient air quality data and dispersion modelling. Internal nickel exposure was assessed by nickel concentrations in morning urine samples of the children. RESULTS: The observed nickel sensitization prevalence rates varied between 12.6% and 30.7%. Statistically significant associations were showed between exposure to nickel in ambient air and urinary nickel concentration as well as between urinary nickel concentration and nickel sensitization. Furthermore, an elevated prevalence of nickel sensitization was associated with exposure to increased nickel concentrations in ambient air. CONCLUSION: The observed associations support the assumption that inhaled nickel in ambient air might be a risk factor for nickel sensitization; further studies in larger collectives are necessary.

Investigations on the estrogenic activity of the metallohormone cadmium in the rat intestine.

Cadmium (Cd), a toxic heavy metal and an important environmental pollutant, is now also regarded as potential endocrine disruptor. Its estrogenic effects have been examined so far just in classical target tissues, e.g. uterus, and mostly upon intraperitoneal (i.p.) injection of CdCl(2). Yet, estrogen receptors are also expressed in the gut, and food is the main source of cadmium intake in the general population. Therefore, possible estrogenic effects were now investigated in the intestine of ovariectomized Wistar rats after oral short- and long-term administration of CdCl(2) (0.05-4 mg/kg bw on 3 days by gavage and 0.4-9 mg/kg bw for 4 weeks in drinking water) or upon i.p. injection (0.00005-2 mg CdCl(2)/kg bw), and compared to steroid estrogen (estradiol or ethinylestradiol) treated groups. Analysis of Cd in kidneys and small intestine by atomic absorption spectrometry showed dose-dependent increases in tissue levels with rather high Cd concentrations in the gut, both after oral and i.p. administration. Expression of metallothionein (MT1a), a typical metal response parameter, was clearly induced in kidney and small intestine of several CdCl(2) treated groups, but also notably increased by steroid estrogens. Levels of estrogen-regulated genes, i.e. pS2/TFF1, vitamin D receptor (VDR), and estrogen receptor alpha and beta (ER alpha/beta) were studied as parameters of hormonal activity: The intestinal mRNA expression of pS2/TFF1 was significantly decreased in the estrogen reference groups, but also after single i.p. injection and oral long-term administration of CdCl(2). In contrast, the mRNA and protein expression of the VDR were unaffected by long-term administration of Cd via drinking water. We detected expression of ERbeta, but not ERalpha in the small intestine of OVX rats. ERbeta mRNA and protein expression were significantly down-regulated by Cd, similar to the ethinylestradiol reference group. The mRNA expression and immunostaining of proliferating cell nuclear antigen (PCNA), as an index for cell proliferation, revealed decreases after long-term administration of Cd and ethinylestradiol. In summary, cadmium exposure was shown to modulate molecular and functional parameters of estrogenicity in the intestinal tract of OVX rats. As the intestine is known to express predominantly ERbeta, and is an important site of interaction with dietary contaminants, it is indicated to further investigate specific molecular mechanisms of cadmium and estrogen receptor interactions in more detail.

Dose- and route-dependent hormonal activity of the metalloestrogen cadmium in the rat uterus.

The toxic heavy metal cadmium (Cd) is regarded as a potential endocrine disruptor, since Cd exerts estrogen-like activity in vitro and can elicit some typical estrogenic responses in rodents upon intraperitoneal (i.p.) injection. But estrogenic effects have not been documented in vivo with other more relevant routes of exposure, although it is known that Cd absorption and distribution in the body is strongly affected by the application route. Therefore, we investigated its hormonal activity in ovariectomized Wistar rats after oral administration of CdCl(2) (0.05-4 mg/kg b.w. on 3 days by gavage and 0.4-9 mg/kg b.w. for 4 weeks in drinking water) in comparison with i.p. injection of CdCl(2) (0.00005-2 mg/kg b.w.). Uterus wet weight, height of uterine epithelium, and modulation of estrogen-regulated gene expression, i.e. uterine complement component 3 (C3), were determined, and also Cd-levels in uterus and liver were measured by atomic absorption spectrometry. The analysis revealed pronounced differences in Cd tissue levels and hormonal potency for the two routes of administration: a single i.p. injection of Cd increased dose-dependently uterine wet weight and thickness of the uterine epithelium. Interestingly, C3 mRNA expression in the uterus was down regulated at low doses of CdCl(2) (0.00005-0.05 mg/kg b.w.), but strongly stimulated at the highest dose of 2 mg/kg b.w. Other than i.p. injection, oral treatment with Cd, by gavage or in drinking water, did neither increase uterine wet weights nor epithelial thickness. But, both 3-day- and 4-week oral Cd administration resulted in a dose-dependent stimulation of C3 expression in the uterus, significant at and above 0.5 mg/kg b.w. In summary, our data demonstrate an estrogenic effect in the uterus upon i.p. injection of Cd, but considerably lower hormonal potency with oral administration: short and long-term oral treatment with Cd did not affect uterus weight or histology, whilst on the molecular level, an induction of estrogen sensitive uterine gene expression was observed, albeit at dose levels far exceeding those of dietary exposure in humans.

Dietary intake of nickel and zinc by young children--results from food duplicate portion measurements in comparison to data calculated from dietary records and available data on levels in food groups.

The daily dietary intake of nickel (Ni) and zinc (Zn) by 42 young children, 21 boys and 21 girls, from 4 to 7 years of age, living in urban and rural areas of Germany and having different food consumption behaviour, was determined by the duplicate method with a 7-day sampling period. Dietary records were also kept by the children's parents for the 7-day sampling period. Individual reported food items were identified, assigned to food groups and, together with known Ni and Zn concentrations of foodstuffs, daily intake rates were calculated. The same method was used for calculations of the energy, fat, protein and carbohydrate intake rates. The levels in the food duplicates, determined by atomic absorption spectrometry, were in the range of 69-2000 microg Ni/kg(dry weight) (geometric mean (GM): 348) and 7.1-43 mg Zn/kg(dry weight) (GM: 17.5). Daily intake rates based on the 294 individual food duplicate analyses were 12-560 microgNi/d (GM: 92.3) and 1.5-11 mgZn/d (GM: 4.63). The results from the dietary records were 35-1050 microg Ni/d (GM: 123) and 1.7-15 mg Zn/d (GM: 5.35). The results of the daily intake rates from both methods showed a correlation with regard to Zn (r=0.56), but no correlation was found between either the Ni intake rates determined with both methods or between the Ni intake rates measured by the duplicate method and calculated intake rates from the dietary records of energy, fat, protein, carbohydrates or drinking water. In the case of nickel, the discrepancies between the methods lead one to suppose that the main factors influencing Ni intake by food are not directly caused by easily assessable food ingredients themselves. It is possible that other factors, such as contaminated drinking water or the transition of Ni from kettles or other household utensils made from stainless steel into the food, may be more relevant. In addition there are some foodstuffs with great variations in concentrations, often influenced by the growing area and environmental factors. Further, some food groups naturally high in Nickel like nuts, cocoa or teas might not have been kept sufficient within the records. In summary, the dietary record method gave sufficient results for Zn, but is insufficient for Ni. Based on the food duplicate analysis, children living in urban areas with consumption of food products from a family-owned garden or the surrounding area and/or products from domestic animals of the surrounding area had about one-third higher Ni levels in their food than children either living in an urban area or children consuming products exclusively from the supermarket. Only slight differences were found with regard to Zn. Compared to the recommendations of the German Society of Nutrition (DGE) (25-30 microgNi/d and 5.0 mgZn/d), the participants of the study had a clearly increased Ni and, in view of the geometric mean value, a nearly adequate Zn intake. Health risks are especially given with regard to the influence of nickel intake by food on dermatitis for nickel-sensitive individuals.

Polychlorinated dibenzo-p-dioxins/polychlorinated dibenzofurans (PCDD/Fs), polychlorinated biphenyls (PCBs), and organochlorine pesticides in human blood of pregnant women from Germany.

Blood samples from 226 pregnant women aged between 19 and 41 yr, living in an industrialized area of Germany (Duisburg birth cohort study), were collected between September 2000 and November 2002 and analyzed for their content of persistent organic pollutants (POPs). Levels of polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and polychlorinated biphenyls (PCBs) were in the range of 4.34-97.3 pg WHO 1998 TEq/g(lipid base) (median: 25.96) or 3.77-63.56 pg WHO 2005 TEq/g(lipid base) (median: 19.38), respectively. Whole blood volume-based concentrations of organochlorine pesticides and their metabolites were 0.036-0.53 microg/L (median: 0.15) hexachlorobenzene (HCB), 4.5-1300 ng/L (median: 67) beta-hexachlorocyclohexane (HCH), 0.6-520 ng/L (median: 18) 4,4'-dichlorodiphenyltrichloroethane (DDT), and 0.1-9.1 microg/L (median: 0.54) 4,4'-dichlorodiphenyldichloroethene (DDE). Parameters influencing the POP levels in human blood were examined using multiple regression models. Levels and the levels scatter widths of most PCDD/F and PCB congeners and HCB increased significantly with age. Within the multiple regression model a weak age dependence was also found for beta-HCH and DDT, whereas blood levels of alpha- and gamma- HCH and DDE were not age dependent. The total lactation period for earlier born children decreased most POP blood levels, except for alpha- and gamma-HCH. Over the study period of 27 mo only a low decreasing effect on human POP blood levels was observed. The body mass index had in general no or a low positive influence on contaminant levels. Because exposure to PCDD/F and PCB is higher in most industrialized countries in comparison to less industrialized ones, lower levels of these substances were detected in blood samples of women who had lived outside Western Europe for a longer period. In contrast, these women showed higher blood levels of organochlorine pesticides, indicating that these chemicals are still in use outside Western Europe.

Environmental exposure to dioxins and polychlorinated biphenyls reduce levels of gonadal hormones in newborns: results from the Duisburg cohort study.

BACKGROUND: Endocrine dysfunction related to the hypothalamic-pituitary-thyroid (HPT) and/or the hypothalamic-pituitary-gonadal axis (HPG) is being discussed as underlying developmental adversity of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) and polychlorinated biphenyls (PCBs). This study was done to evaluate effects related to the HPG axis. METHODS: A birth-cohort study was initiated in the year 2000. Healthy mother-infant pairs were recruited in the industrialized city of Duisburg, Germany. Dioxins, dioxin-like PCBs and six indicator PCBs were measured in maternal blood during pregnancy and in maternal milk. Testosterone and estradiol levels were measured in maternal and cord serum of 104 mother-infant pairs representing a subsample with a complete data set of the total basic sample of 232 participants. Linear regression analysis was used to describe the association of PCDD/Fs or PCB in maternal blood or milk with sex steroid concentrations after adjustment for confounding. RESULTS: Median concentrations for PCDD/Fs in maternal blood fat and milk fat in terms of WHO-TEq were 15.3 and 13.1pg WHO-TEq/g, respectively, and for the sum of the indicator PCBs (#28, #52, #101, #138, #153, #180) 149 and 177ng/g. The adjusted ratio of geometric means when doubling the concentration of PCDD/Fs in maternal blood fat was 0.86, 95% confidence interval (95% CI): 0.72-1.03 for testosterone and 0.73 (0.61-0.87) for estradiol in cord serum. Typically, testosterone reduction was more pronounced in cord serum of female and estradiol reduction in that of male babies. Reduction of hormone levels was generally more pronounced for dioxins than for indicator PCBs. CONCLUSIONS: The hypothalamic-pituitary-gonadal axis of newborn babies is influenced by prenatal exposure to PCDD/Fs and PCBs in a manner suggestive of AhR-mediation. The clinical relevance of this finding remains to be established, however.

Consumption of homegrown products does not increase dietary intake of arsenic, cadmium, lead, and mercury by young children living in an industrialized area of Germany.

The dietary intake of arsenic (As), cadmium (Cd), mercury (Hg), and lead (Pb) was studied among young German children with different food consumption behaviour (consumption of own grown foodstuffs and of products from the supermarket). The study area comprised an industrialized and a rural area of West Germany. Dietary intake of contaminants was measured by the duplicate method according to the WHO guideline. A total 588 duplicate portions were collected daily from 84 individuals between May and September 1998. Intake of food groups was calculated from dietary records. Determination of As, Cd, Hg, and Pb was performed following high-pressure digestion of lyophilized samples by atomic absorption spectrometry (AAS). Geometric mean weekly intake [microg/(kgbw x week)] was as follows: As 1.4, Cd 2.3, Hg 0.16, and Pb 5.3. Geometric mean intake corresponded to the percentage of the provisional tolerable weekly intake (PTWI) as follows: As 9.7%, Cd 32%, Hg 3.3%, Pb 21%. As and Hg intake were mainly influenced by fish consumption. The amount of cereals and bakery wares mainly determined the Cd and Pb intake. Children living in the industrialized area with a substantial food consumption of own grown vegetables or products from domestic animals products had no increased dietary intake of the metals.

Dietary intake of cadmium by children and adults from Germany using duplicate portion sampling.

The dietary intake of cadmium was studied among children and adults from Germany. The study area comprised the highly industrialized Ruhr district as well as the North Sea island Amrum. A total of 229 duplicate samples were collected from 49 individuals between December 1994 and May 1995. The sampling period for each participant was either 3 or 7 days. Cadmium concentrations in duplicate samples were measured by atomic absorption spectrometry. The daily cadmium intakes (geometric mean) for 4 different groups of individuals distributed as follows: for small children (mean age: 1.8 years) from the Ruhr district 0.17 microg/(kg(bw) x day) [range: 0.02-1.62 microg/(kg(bw) x day)], for children (mean age: 3.8 years) from the Ruhr district 0.49 microg/(kg(bw) x day) [range: 0.11-2.06 microg/(kg(bw) x day)], for children (mean age: 3.9 years) living on the North Sea island Amrum 0.35 microg/(kg(bw)-day) [range: 0.09-1.13 microg/ (kg(bw) x day)] and for adults (mean age: 40.9 years) from the Ruhr district 0.37 microg/(kg(bw) x day) [range: 0.05-1.32 microg/(kg(bw) x day)]. Compared to the provisional tolerable weekly intake (PTWI) of 7 microg/(kg(bw) x week) proposed by the WHO the dietary intake of cadmium was rather high. The geometric mean and maximum intake values for the different groups ranged between 24.3-55.7% and 62.7-120.7 respectively of the PTWI. We therefore conclude, that the cadmium exposure of the population needs to be reduced in order to minimize the risk of adverse health effects related to this metal.