Indoor Mold.

BACKGROUND: According to self-reported frequencies, every fifth or sixth dwelling in Germany is affected by dampness and/or mold. This carries a potential risk to health. METHODS: This review is based on pertinent publications retrieved by a selective literature search and inquiry in the GENESIS database, on the AWMF guideline on the medical clinical diagnosis of indoor mold exposure, as updated in 2023, and on the relevant contents of other current guidelines. Based on this research, we present an algorithm for the evaluation of health problems that may be due to mold in indoor environments. RESULTS: A rational diagnostic work-up begins with history-taking and physical examination, with attention to risk factors-above all, immune compromise and atopy. If there is evidence of atopy, targeted allergy diagnostics should be performed, consisting of a skin prick test and/or measurement of specific IgE antibodies, supplemented whenever indicated by provocative testing and cellular test systems. If the patient's immune response is compromised, the immediate cessation of mold exposure has absolute priority. Any suspected invasive fungal infection should be evaluated with radiological, microbiological, serological, and immunological testing. Indoor measurements of mold fungi, microbial volatile organic compounds (MVOC), and/or mycotoxins are generally not indicated as part of the medical evaluation; nor are blood or urine tests for particular mold components or metabolites. CONCLUSION: Mold in indoor environments should be dealt with by rapid exposure elimination for patients at risk, the rational diagnostic evaluation of any symptoms and signs of disease, and patient education about the possibilities and limitations of diagnostic testing and the generally limited utility of measurements in the affected interior spaces.

AWMF mold guideline "Medical clinical diagnostics for indoor mold exposure" - Update 2023 AWMF Register No. 161/001.

None.

Partition of environmental chemicals between maternal and fetal blood and tissues.

Passage of environmental chemicals across the placenta has important toxicological consequences, as well as for choosing samples for analysis and for interpreting the results. To obtain systematic data, we collected in 2000 maternal and cord blood, cord tissue, placenta, and milk in connection with births in the Faroe Islands, where exposures to marine contaminants is increased. In 15 sample sets, we measured a total of 87 environmental chemicals, almost all of which were detected both in maternal and fetal tissues. The maternal serum lipid-based concentrations of organohalogen compounds averaged 1.7 times those of cord serum, 2.8 times those of cord tissue and placenta, and 0.7 those of milk. For organohalogen compounds detectable in all matrices, a high degree of correlation between concentrations in maternal serum and the other tissues investigated was generally observed (r(2) > 0.5). Greater degree of chlorination resulted in lower transfer from maternal serum into milk. Concentrations of pentachlorbenzene, γ-hexachlorocyclohexane, and several polychlorinated biphenyl congeners with low chlorination were higher in fetal samples and showed poor correlation with maternal levels. Perfluorinated compounds occurred in lower concentrations in cord serum than in maternal serum. Cadmium, lead, mercury, and selenium were all detected in fetal samples, but only mercury showed close correlations among concentrations in different matrices. Although the environmental chemicals examined pass through the placenta and are excreted into milk, partitions between maternal and fetal samples are not uniform.

A controlled challenge study on di(2-ethylhexyl) phthalate (DEHP) in house dust and the immune response in human nasal mucosa of allergic subjects.

BACKGROUND: Few studies have yet addressed the effects of di(2-ethylhexyl) phthalate (DEHP) in house dust on human nasal mucosa. OBJECTIVES: We investigated the effects of house dust containing DEHP on nasal mucosa of healthy and house dust mite (HDM)-allergic subjects in a short-term exposure setting. METHODS: We challenged 16 healthy and 16 HDM-allergic subjects for 3 hr with house dust at a concentration of 300 microg/m(3) containing either low (0.41 mg/g) or high (2.09 mg/g) levels of DEHP. Exposure to filtered air served as control. After exposure, we measured proteins and performed a DNA microarray analysis. RESULTS: Nasal exposure to house dust with low or high DEHP had no effect on symptom scores. Healthy subjects had almost no response to inhaled dust, but HDM-allergic subjects showed varied responses: DEHP(low) house dust increased eosinophil cationic protein, granulocyte-colony-stimulating factor (G-CSF), interleukin (IL)-5, and IL-6, whereas DEHP(high) house dust decreased G-CSF and IL-6. Furthermore, in healthy subjects, DEHP concentration resulted in 10 differentially expressed genes, whereas 16 genes were differentially expressed in HDM-allergic subjects, among them anti-Müllerian hormone, which was significantly up-regulated after exposure to DEHP(high) house dust compared with exposure to DEHP(low) house dust, and fibroblast growth factor 9, IL-6, and transforming growth factor-beta1, which were down-regulated. CONCLUSIONS: Short-term exposure to house dust with high concentrations of DEHP has attenuating effects on human nasal immune response in HDM-allergic subjects, concerning both gene expression and cytokines.

Differential response of Mono Mac 6, BEAS-2B, and Jurkat cells to indoor dust.

BACKGROUND: Airway toxicity of indoor dust is not sufficiently understood. OBJECTIVES: Our goal in this study was to describe the effects of indoor dust on human monocyte, epithelial, and lymphocyte cell lines. We aimed to a) obtain a comprehensive and intelligible outline of the transcriptional response; b) correlate differential transcription with cellular protein secretion; c) identify cell line-specific features; and d) search for indoor dust-specific responses. METHODS: Settled dust was sampled in 42 German households, and various contaminants were characterized. We exposed Mono Mac 6, BEAS-2B, and Jurkat cells to 500 microg/mL indoor dust for 6 hr. Outcome parameters included the transcriptional profile of an oligonucleotide microarray covering 1,232 genes. Significantly enriched Gene Ontology themes were calculated. Supernatant protein levels of 24 inflammatory response proteins served to confirm transcriptional results. RESULTS: An intraclass correlation coefficient of 0.8 indicated reasonable microarray reproducibility. The transcriptional profile was characterized by enhancement of detoxification and a danger and defense response. Differential gene regulation correlated with protein secretion (Goodman and Kruskal's gamma coefficient: 0.72; p < 0.01). Mono Mac 6 cells revealed the highest fraction of differentially expressed genes, dominated by up-regulation of various cytokines and chemokines. BEAS-2B cells revealed weaker changes in a limited set of inflammatory response proteins. No significant changes were observed in Jurkat cells. CONCLUSIONS: Monocytes are particularly responsive to indoor dust. We observed a classical T-helper 1-dominated immune response, which suggested that bioorganic contaminants are relevant effectors in indoor dust.

PCB and dioxin-like PCB in indoor air of public buildings contaminated with different PCB sources--deriving toxicity equivalent concentrations from standard PCB congeners.

Data on dioxin-like PCB in indoor air of buildings with PCB-containing materials and on possible correlation between toxicity equivalent concentrations (TEQ) and levels of non-dioxin-like standard PCB is sparse. As part of a larger survey on indoor-air contamination with PCB, the connection between the concentration of standard PCB congeners and the dioxin-like toxicity expressed as TEQ was investigated. Indoor air samples (n=8) were collected in four public buildings with known PCB sources and total PCB levels in the range from 715 to 2250 ng/m3 and analyzed for the six non-dioxin-like standard PCB (congeners 28, 52, 101, 138, 153, 180), the twelve dioxin-like PCB congeners according to WHO and the 17 2,3,7,8-substituted PCDD/PCDF congeners. In three buildings where PCB were used as flame retardant coatings of acoustic ceiling tiles, PCB 101 had the maximum level among the six standard PCB, while in the building with permanent elastic sealants as PCB source, congeners 28 and 52 dominated the pattern by far. In the case of permanent elastic sealants as PCB source (n=3) a total PCB concentration of 1000 ng/m3 corresponded to a total TEQ level of 0.3-0.6 pg/m3. In contrast, in rooms with acoustic ceiling tiles as PCB source, 1.8-4.7 pg TEQ/m3 per 1000 ng total PCB/m3 were found. Linear regression analysis between PCB and TEQ indicated that PCB 118 might be used to calculate the total TEQ of dioxin-like PCB and PCDD/PCDF. By means of such a correlation it is possible to estimate TEQ by extrapolation from the results of less sophisticated analytical methods. It is tentatively recommended to use PCB 118 for screening purposes or re-evaluation of standard PCB indoor-air measurements. If only the six non-dioxin-like PCB standard congeners are available, a regression algorithm using the sum of PCB 101, 138, 153 and 180 might be used instead.

Medical diagnostics for indoor mold exposure.

In April 2016, the German Society of Hygiene, Environmental Medicine and Preventative Medicine (Gesellschaft für Hygiene, Umweltmedizin und Präventivmedizin (GHUP)) together with other scientific medical societies, German and Austrian medical societies, physician unions and experts has provided an AWMF (Association of the Scientific Medical Societies) guideline 'Medical diagnostics for indoor mold exposure'. This guideline shall help physicians to advise and treat patients exposed indoors to mold. Indoor mold growth is a potential health risk, even without a quantitative and/or causal association between the occurrence of individual mold species and health effects. Apart from the allergic bronchopulmonary aspergillosis (ABPA) and the mycoses caused by mold, there is only sufficient evidence for the following associations between moisture/mold damages and different health effects: Allergic respiratory diseases, asthma (manifestation, progression, exacerbation), allergic rhinitis, exogenous allergic alveolitis and respiratory tract infections/bronchitis. In comparison to other environmental allergens, the sensitizing potential of molds is estimated to be low. Recent studies show a prevalence of sensitization of 3-10% in the total population of Europe. The evidence for associations to mucous membrane irritation and atopic eczema (manifestation, progression, exacerbation) is classified as limited or suspected. Inadequate or insufficient evidence for an association is given for COPD, acute idiopathic pulmonary hemorrhage in children, rheumatism/arthritis, sarcoidosis, and cancer. The risk of infections from indoor molds is low for healthy individuals. Only molds that are capable to form toxins can cause intoxications. The environmental and growth conditions and especially the substrate determine whether toxin formation occurs, but indoor air concentrations are always very low. In the case of indoor moisture/mold damages, everyone can be affected by odor effects and/or impairment of well-being. Predisposing factors for odor effects can be given by genetic and hormonal influences, imprinting, context and adaptation effects. Predisposing factors for impairment of well-being are environmental concerns, anxieties, conditioning and attributions as well as a variety of diseases. Risk groups that must be protected are patients with immunosuppression and with mucoviscidosis (cystic fibrosis) with regard to infections and individuals with mucoviscidosis and asthma with regard to allergies. If an association between mold exposure and health effects is suspected, the medical diagnosis includes medical history, physical examination, conventional allergy diagnosis, and if indicated, provocation tests. For the treatment of mold infections, it is referred to the AWMF guidelines for diagnosis and treatment of invasive Aspergillus infections. Regarding mycotoxins, there are currently no validated test methods that could be used in clinical diagnostics. From the perspective of preventive medicine, it is important that mold damages cannot be tolerated in indoor environments.

Abridged version of the AWMF guideline for the medical clinical diagnostics of indoor mould exposure: S2K Guideline of the German Society of Hygiene, Environmental Medicine and Preventive Medicine (GHUP) in collaboration with the German Association of Allergists (AeDA), the German Society of Dermatology (DDG), the German Society for Allergology and Clinical Immunology (DGAKI), the German Society for Occupational and Environmental Medicine (DGAUM), the German Society for Hospital Hygiene (DGKH), the German Society for Pneumology and Respiratory Medicine (DGP), the German Mycological Society (DMykG), the Society for Pediatric Allergology and Environmental Medicine (GPA), the German Federal Association of Pediatric Pneumology (BAPP), and the Austrian Society for Medical Mycology (ÖGMM).

This article is an abridged version of the AWMF mould guideline "Medical clinical diagnostics of indoor mould exposure" presented in April 2016 by the German Society of Hygiene, Environmental Medicine and Preventive Medicine (Gesellschaft für Hygiene, Umweltmedizin und Präventivmedizin, GHUP), in collaboration with the above-mentioned scientific medical societies, German and Austrian societies, medical associations and experts. Indoor mould growth is a potential health risk, even if a quantitative and/or causal relationship between the occurrence of individual mould species and health problems has yet to be established. Apart from allergic bronchopulmonary aspergillosis (ABPA) and mould-caused mycoses, only sufficient evidence for an association between moisture/mould damage and the following health effects has been established: allergic respiratory disease, asthma (manifestation, progression and exacerbation), allergic rhinitis, hypersensitivity pneumonitis (extrinsic allergic alveolitis), and increased likelihood of respiratory infections/bronchitis. In this context the sensitizing potential of moulds is obviously low compared to other environmental allergens. Recent studies show a comparatively low sensitizing prevalence of 3-10% in the general population across Europe. Limited or suspected evidence for an association exist with respect to mucous membrane irritation and atopic eczema (manifestation, progression and exacerbation). Inadequate or insufficient evidence for an association exist for chronic obstructive pulmonary disease, acute idiopathic pulmonary hemorrhage in children, rheumatism/arthritis, sarcoidosis and cancer. The risk of infection posed by moulds regularly occurring indoors is low for healthy persons; most species are in risk group 1 and a few in risk group 2 (Aspergillus fumigatus, A. flavus) of the German Biological Agents Act (Biostoffverordnung). Only moulds that are potentially able to form toxins can be triggers of toxic reactions. Whether or not toxin formation occurs in individual cases is determined by environmental and growth conditions, above all the substrate. In the case of indoor moisture/mould damage, everyone can be affected by odour effects and/or mood disorders. However, this is not a health hazard. Predisposing factors for odour effects can include genetic and hormonal influences, imprinting, context and adaptation effects. Predisposing factors for mood disorders may include environmental concerns, anxiety, condition, and attribution, as well as various diseases. Risk groups to be protected particularly with regard to an infection risk are persons on immunosuppression according to the classification of the German Commission for Hospital Hygiene and Infection Prevention (Kommission für Krankenhaushygiene und Infektionsprävention, KRINKO) at the Robert Koch- Institute (RKI) and persons with cystic fibrosis (mucoviscidosis); with regard to an allergic risk, persons with cystic fibrosis (mucoviscidosis) and patients with bronchial asthma should be protected. The rational diagnostics include the medical history, physical examination, and conventional allergy diagnostics including provocation tests if necessary; sometimes cellular test systems are indicated. In the case of mould infections the reader is referred to the AWMF guideline "Diagnosis and Therapy of Invasive Aspergillus Infections". With regard to mycotoxins, there are currently no useful and validated test procedures for clinical diagnostics. From a preventive medicine standpoint it is important that indoor mould infestation in relevant dimension cannot be tolerated for precautionary reasons. With regard to evaluating the extent of damage and selecting a remedial procedure, the reader is referred to the revised version of the mould guideline issued by the German Federal Environment Agency (Umweltbundesamt, UBA).

Effects of developmental co-exposure to methylmercury and 2,2',4,4',5,5'-hexachlorobiphenyl (PCB153) on cholinergic muscarinic receptors in rat brain.

The developing nervous system is thought to be particularly sensitive to polychlorinated biphenyls (PCBs) present as food contaminants together with methylmercury (MeHg). Effects of perinatal co-exposure to PCB153 and MeHg on brain cholinergic muscarinic receptors (MRs) were investigated by saturation binding studies in mature and immature rats. MeHg alone (1mg/kg/day, GD7-PND7) enhanced cerebral MRs more in dams (87% and 60% in cerebellum and cerebral cortex, respectively) than in PND21 pups (0-50%) in accordance with the higher Hg levels detected in the adult brain (7-9 microg/g) than in the male and female offspring's brain (1.5-2.8 microg/g). Prenatal administration of PCB153 (20mg/kg/day, GD10-GD16), leading to higher contaminant levels in the offspring brain than in that of adults (25-66 microg/g versus 3 microg/g), induced cerebral MR changes of similar extent at both ages, namely decreased cerebellar (20-30%) and increased cortical MR density (40-50%). Co-exposure to PCB and MeHg had no more effect than exposure to either compound alone on cerebral cortex MRs, whereas, in the cerebellum, the combined treatment induced a PCB-like lowering of the MR density that masked the MeHg-induced receptor increase. None of the treatments affected the striatal and hippocampal MRs. A lower MeHg dose (0.5 mg/kg/day) was without any effect on cerebral MRs. These results show that MRs are one of the sensitive biochemical endpoints of the central nervous system altered by developmental exposure to MeHg and PCB153. Cerebral cortex and cerebellum were the most susceptible targets in the response to these neurotoxicants. MR changes were detected in both immature and adult animals and the interaction of MeHg and PCB153 at the level of these receptors occurred in a non-additive manner.

Indoor air guide values for glycol ethers and glycol esters-A category approach.

The German Committee on Indoor Guide Values issues indoor air guide values to protect public health. For health evaluation of glycol ethers and glycol esters in air, the entire group of substances with data for 47 chemicals was analyzed in order to gain a consistent assessment. For some glycol ethers reproductive and hematological effects are of central interest, whereas for others effects on liver and kidneys are crucial. Moreover, some glycol ethers have also been shown to cause irritation of the respiratory tract. For 14 chemicals, suitable inhalation studies were available for deriving specific guide values, or analogies to closely related substances could be drawn. For these chemicals individual indoor air guide values were derived, the respective guide value I ranging from 0.02 to 2mg/m(3). Guide values were derived according to the procedures issued by the Committee, considering the exposure duration in indoor air compared to animal studies or the situation at workplaces, the duration of the respective study, species differences, and interindividual variability including special sensitivity of children. For glycol ethers with insufficient data default guide values II and I of 0.05 and 0.005ppm, respectively, were recommended based on statistical analyses of the available data on all glycol ethers and on evaluation of single studies. For evaluation of combined effects additivity is assumed.

Attenuated growth of breast-fed children exposed to increased concentrations of methylmercury and polychlorinated biphenyls.

Breast-feeding has been linked to slowed postnatal growth. Although the basis for this "weanling's dilemma" is unclear, environmental contaminants in human milk may be of relevance. We studied a Faroese birth cohort of 182 singleton children, born at term in 1994-95. Concentrations of mercury in cord blood and of polychlorinated biphenyls in maternal milk were measured, and duration of breast-feeding was recorded. At 18 months, children who had been exclusively breast-fed for at least 6 months weighed 0.59 kg less [95% confidence interval (CI) = 0.03, 1.16 kg] and were 1.50 cm [95% CI = 0.52, 2.47 cm] shorter than those not breast-fed. However, calculated transfer of contaminants from human milk fully explained the attenuated growth. Irrespective of duration of breast-feeding, a doubling of the mercury concentration in cord blood was associated with a decrease in weight at 18 months by 0.19 kg (95% CI = 0.03, 0.35 kg) and in height by 0.26 cm (95% CI = -0.02, 0.55 cm). Weight and height at 42 months showed the same tendencies, but the main effect occurred before 18 months of age. Thus, in communities with increased contaminant exposures, risks associated with lactational transfer of toxicants to the infant must be considered when judging the benefits of prolonged breast-feeding.

PCB-related neurodevelopmental deficit may be transient: follow-up of a cohort at 6 years of age.

UNLABELLED: Based on our own findings from a previous study we aimed to establish if cognitive deficit, shown to be induced by perinatal exposure to polychlorinated biphenyls (PCBs) at earlier ages, persists into school-age. Seventy-seven percent of a cohort last examined at 42 months of age using the Kaufman Assessment Battery for Children were reexamined with the same test at 72 months. At this point, and contrary to the results at 30 and 42 months no adverse PCB-effects were found. However, the positive effect of the home environment became even more pronounced. CONCLUSION: early PCB-exposure at current environmental background levels possibly induces transient delay in cognitive development rather than irreversible deficit.

Comparison of polychlorinated biphenyl levels across studies of human neurodevelopment.

Polychlorinated biphenyls (PCBs) are persistent pollutants that are ubiquitous in the food chain, and detectable amounts are in the blood of almost every person in most populations that have been examined. Extensive evidence from animal studies shows that PCBs are neurotoxins, even at low doses. Interpretation of human data regarding low-level, early-life PCB exposure and subsequent neurodevelopment is problematic because levels of exposure were not similarly quantified across studies. We expressed the exposure levels from 10 studies of PCB and neurodevelopment in a uniform manner using a combination of data from original investigators, laboratory reanalyses, calculations based on published data, and expert opinion. The mainstay of our comparison was the median level of PCB 153 in maternal pregnancy serum. The median concentration of PCB 153 in the 10 studies ranged from 30 to 450 ng/g serum lipid, and the median of the 10 medians was 110 ng/g. We found that (a)) the distribution of PCB 153 exposure in most studies overlapped substantially, (b)) exposure levels in the Faroe Islands study were about 3-4-fold higher than in most other studies, and (c)) the exposure levels in the two recent U.S. studies were about one-third of those in the four earlier U.S. studies or recent Dutch, German, and northern Québec studies. Our results will facilitate a direct comparison of the findings on PCBs and neurodevelopment when they are published for all 10 studies.

Pollutants in house dust as indicators of indoor contamination.

This review summarizes occurrence of organic and inorganic contaminants in house dust and the contribution of house dust as a marker of indoor exposure. Several studies have identified house dust as an important route of toxicant exposure. Often levels of pollutants found in house dust, including compounds banned long ago, are significant sources of exposure for the general population, especially children. House dust is a sink and repository for semivolatile organic compounds and particle-bound matter. Analyses of compounds in house dust are a measure of indoor contamination but may also provide valuable information for assessment of human indoor exposure. The objective of analyzing house dust are to describe the extent, distribution, and determinants of exposure, to identify possible sources of indoor contamination, or to record elevated indoor exposure leading to intervention or sanitation. House dust and compounds adsorbed to house dust may enter the human body by inhalation of suspended and resuspended particles, through nondietary ingestion of dust, through ingestion of particles adhering to food, surfaces in the homes, and on the skin as well as by absorption through the skin. The quantity of dust inhaled and deposited in the differing parts of the alveolar tract is dependent on the aerodynamic diameter. Exposure to house dust does not exclusively and may not even predominantly occur via inhalation, however. For instance, ingestion of house dust particles adhering to food, objects, and the skin or direct absorption through the skin may be primary routes of exposure (Lewis et al. 1994). Samples referred to as "house dust" vary significantly because house dust may be of different origin, amount, and composition and the method of sampling the dust influences the properties of the sample used for analysis. Passive and active sampling methods are described and discussed. For the analysis of organic pollutants in house dust, the < or = 63-microns fraction should be favored because variances caused by inhomogeneity of the subsample are low. Results from studies on house dust are presented for polychlorinated biphenyls (PCB), polycyclic aromatic hydrocarbons (PAH), plasticizers (phthalates, phenols), flame retardants, other organic xenobiotics, and inorganic constituents. If available, medians as a measure of the average concentration and the 90th or 95th percentiles are added as reference values. The review of the literature points out that ingestion of house dust may be a major route of exposure to pesticides for infants and toddlers. So far, only a few guideline values or limiting values for house dust exist. For lead in house dust, the health risk is regulated only in the U.S. and for PAH in the Federal Republic of Germany. Risk associated with the ingestion of contaminated dust by small children (age, 1-6 years; mean body weight, 16 kg) can be estimated using the chronic oral reference dose (RfD) and a daily intake of 100 mg house dust. The tentative benchmark house dust concentrations that are believed to be without health effect for small children were calculated for several compounds from their current RfD. Comparison with the maximum concentrations reviewed for chlorpyrifos, DDT, and diazinon indicates that the tolerable exposure concentration in house dust might be exceeded and that chlorpyrifos especially can be considered as a potential hazard to householders. The role of house dust as an exposure source is gaining more attention over the years but several open questions related to health remain to be resolved. Pesticides applied outside or within the household that are absorbed and preserved by house dust can lead through the everyday activities of children and infants to increased exposure. Residential exposure including house dust residues contribute to combined exposure from dietary and nondietary sources. It is justified to shift more attention to indoor pollution by house dust contamination and to improve the risk assessment of nondietary ingestion, but any health-based standard must be accompanied by a specific dust sampling method.

Dietary intake of persistent organic pollutants (POPs) by German children using duplicate portion sampling.

The dietary intake of persistent organic pollutants (POPs) was studied in 14 German children at the age of 1.5 to 5.3 years from the North Sea island Amrum. A total of 98 duplicate samples were collected between April and May 1995. The sampling period for each participant was 7 days. Concentrations of POPs were measured by capillary gas chromatography and electron capture detection. The median daily intake [ng/(kgbw.day)] for the different compounds were as follows: 1.9 for alpha-HCH, 1.2 for beta-HCH, 9.5 for gamma-HCH, 4.6 for HCB, 3.4 for DDT, 11.2 for DDE, 1.1 for PCB 101, 5.1 for, PCB 138, 5.2 for PCB 153 and 2.2 for PCB 180. Compared to acceptable or tolerable daily intake (ADI/TDI) proposed by WHO and other organizations the dietary intake of POPs was low. The median values of the ADI/TDI for the POPs was less than 2.2%. The highest percentage of tolerable intake was found for the sum of PCB and amounted to 20.4%. However, compared with minimal risk levels (ATSDR), the percentage of dietary intake was much higher, especially for gamma-HCH (based on median intake: 95%), for HCB (23.1%) and for PCB (69%).

Neurobehavioral deficits at age 7 years associated with prenatal exposure to toxicants from maternal seafood diet.

To determine the possible neurotoxic impact of prenatal exposure to polychlorinated biphenyls (PCBs), we analyzed banked cord blood from a Faroese birth cohort for PCBs. The subjects were born in 1986-1987, and 917 cohort members had completed a series of neuropsychological tests at age 7 years. Major PCB congeners (118, 138, 153, and 180), the calculated total PCB concentration, and the PCB exposure estimated in a structural equation model showed weak associations with test deficits, with statistically significant negative associations only with the Boston Naming test. Likewise, neither hexachlorobenzene nor p,p'-dichlorodiphenyldichloroethylene showed clear links to neurobehavioral deficits. Thus, these associations were much weaker than those associated with the cord-blood mercury concentration, and adjustment for mercury substantially attenuated the regression coefficients for PCB exposure. When the outcomes were joined into motor and verbally mediated functions in a structural equation model, the PCB effects remained weak and virtually disappeared after adjustment for methylmercury exposure, while mercury remained statistically significant. Thus, in the presence of elevated methylmercury exposure, PCB neurotoxicity may be difficult to detect, and PCB exposure does not explain the methylmercury neurotoxicity previously reported in this cohort.

Human biomonitoring assessment values: approaches and data requirements.

Human biomonitoring (HBM) data is a very useful metric for assessing human's exposures to chemicals in commerce. To assess the potential health risks associated with the presence of chemicals in blood, urine or other biological matrix requires HBM assessment values. While HBM assessment values based on human exposure-response data remain the most highly valuable and interpretable assessment values, enough data exists for such values for very few chemicals. As a consequence, efforts have been undertaken to derive HBM assessment values in which external dose based guidance values such as tolerable daily intakes have been translated into equivalent biomonitoring levels. The development of HBM values by the German HBM Commission and Biomonitoring Equivalents by Summit Toxicology has resulted in conceptually similar assessment values. The review of the development of these values provided here demonstrates examples and approaches that can be used to broaden the range of chemicals for which such assessment values can be derived. Efforts to date have resulted in the publication of HBM assessment values for more than 80 chemicals, and now provide tools that can be used for the evaluation of HBM data across chemicals and populations.

Reassessment of critical lead effects by the German Human Biomonitoring Commission results in suspension of the human biomonitoring values (HBM I and HBM II) for lead in blood of children and adults.

In Germany, the Human Biomonitoring Commission of the Federal Environment Agency continuously assesses environmental pollutants to derive human biomonitoring (HBM) and reference values. HBM values are derived on the basis of toxicological, epidemiological studies or toxicokinetic extrapolation which provides a concentration of a substance or its metabolites corresponding to tolerable intake doses. Two levels are defined: HBM I and HBM II. In 1996, the Commission set a HBM I of 100 microg/l for lead in blood of children < or =12 years and females of a reproductive age and a HBM I of 150 microg/l for the other persons. In the light of findings from epidemiological studies on effects below 100 microg/l, the Commission reevaluated and confirmed the assessment from 1996 in 2002. Meanwhile the general decline in lead pollution has allowed recent studies to include more cohorts with blood lead levels predominantly below 100 microg/l. These data confirm that lead's critical effect, particularly on the developing organism and during early childhood, concerns the nervous system and that negative correlations between blood lead levels and relevant variables (cognitive function, behaviour) occur at blood lead levels below 100 microg/l. The new data also support the possible persistence of lead-induced effects into adulthood. It is not possible to indicate thresholds. Concerning the estimation of the size of the effects, recent studies suggest that lead's influence on development is comparable with other factors influencing development. Furthermore inorganic lead and compounds were classified by IARC in group 2A (probably carcinogenic to humans) and by the German Research Foundation (MAK Commission) in category 2 (to be regarded as human carcinogen). We conclude that any setting of an "effect threshold" for blood lead levels would be arbitrary and therefore unjustified. As a consequence the Commission suspends the HBM values for lead in blood of children and adults.