[show abstract][hide abstract] ABSTRACT: Domestic wood combustion and traffic are the two most significant primary fine particulate matter (PM2.5) emission source categories in Finland. We estimated emission–exposure relationships for primary PM2.5 emissions from these source categories using intake fractions (iF), which describes the fraction of an emission that is ultimately
inhaled by a target population. The iFs were calculated for four different emission source subcategories in Finland in 2000:
(1) domestic wood combustion in residential buildings, (2) domestic wood combustion in recreational buildings, (3) traffic
exhaust and wear emissions, and (4) traffic resuspension emissions. The iFs were estimated for both total population and for
subpopulations with different gender, age, and educational status. Primary PM2.5 emissions were based on the Finnish Regional Emission Scenario model and the dispersion of particles was calculated using
the Urban Dispersion Modeling system of Finnish Meteorological Institute. Both emissions and dispersion were estimated on
a 1 km spatial resolution. The iFs for primary PM2.5 emissions from (1) residential and (2) recreational buildings were 3.4 and 0.6 per million, respectively. The corresponding
iF for (3) traffic exhaust and wear and (4) traffic resuspension emissions were 9.7 and 9.5 per million, respectively. The
differences in population-weighted outdoor concentrations were significant between subpopulations with different educational
status so that people with higher education were exposed more to traffic-related PM2.5.
Air Quality Atmosphere & Health 01/2011; · 1.98 Impact Factor
[show abstract][hide abstract] ABSTRACT: All market participants (e.g., investors, producers, consumers) accept a certain level of risk as necessary to achieve certain benefits. There are many types of risk including price, production, financial, institutional, and individual human risks. All these risks should be effectively managed in order to derive the utmost of benefits and avoid disruption and/or catastrophic economic consequences for the food industry. The identification, analysis, determination, and understanding of the benefit–risk trade-offs of market participants in the food markets may help policy makers, financial analysts and marketers to make well-informed and effective corporate investment strategies in order to deal with highly uncertain and risky situations.
In this paper, we discuss the role that benefits and risks play in the formation of the decision-making process of market-participants, who are engaged in the upstream and downstream stages of the food supply chain. In addition, we review the most common approaches (expected utility model and psychometrics) for measuring benefit–risk trade-offs in the economics and marketing-finance literature, and different factors that may affect the economic behaviour in the light of benefit–risk analyses.
Building on the findings of our review, we introduce a conceptual framework to study the benefit–risk behaviour of market participants. Specifically, we suggest the decoupling of benefits and risks into the separate components of utilitarian benefits, hedonic benefits, and risk attitude and risk perception, respectively. Predicting and explaining how market participants in the food industry form their overall attitude in light of benefit–risk trade-offs may be critical for policy-makers and managers who need to understand the drivers of the economic behaviour of market participants with respect to production, marketing and consumption of food products.
Food and Chemical Toxicology 01/2011; · 3.01 Impact Factor
[show abstract][hide abstract] ABSTRACT: A probabilistic long-term intake estimation of dioxins was carried out using food consumption data obtained from the National FINDIET 2007 Survey (Paturi et al. 2008). The study population consisted of 606 participants who were first interviewed with a 48-h recall and then filled in a 3-day food record twice. The concentrations of dioxins were obtained from previously published studies. The intake was estimated using a semi-parametric Monte Carlo simulation. The analyses were done separately for the whole study population and for the population excluding energy under-reporters. To diminish the impact of intra-individual variation and nuisance effects, adjustment with software (C-SIDE) was also done after Monte Carlo simulation. It was found that when C-SIDE was used, the 95th percentile of intake and its confidence limit was higher with 2 reporting days than with a higher number of days. However, with a crude intake estimation (no adjustment), the confidence intervals of the 95th percentile were also smaller with a higher number of days, but the 95th percentiles were higher with a higher number of reporting days. When under-reporters were excluded the intakes increased, but the impact of energy under-reporting was smaller with 8 reporting days than with 2 days and smaller using C-SIDE than with a crude estimation. To conclude, adjustment for intra-individual variation and taking energy under-reporting into account are essential for intake estimation of dioxins with food consumption data of a limited number of reporting days.
Food Additives and Contaminants - Part A Chemistry, Analysis, Control, Exposure and Risk Assessment 08/2010; 27(8):1170-6.
[show abstract][hide abstract] ABSTRACT: Both industrial chemicals and environmental pollutants can interfere with bone modeling and remodeling. Recently, detailed toxicological bone studies have been performed following exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), which exerts most of its toxic effects through the aryl hydrocarbon receptor (AhR).
The aims of the present study were to quantitatively evaluate changes in bone geometry, mineral density and biomechanical properties following long-term exposure to TCDD, and to further investigate the role of AhR in TCDD-induced bone alterations. To this end, tissue material used in the study was derived from TCDD-exposed Long-Evans (L-E) and Han/Wistar (H/W) rats, which differ markedly in sensitivity to TCDD-induced toxicity due to a strain difference in AhR structure.
Ten weeks old female L-E and H/W rats were administered TCDD s.c. once per week for 20 weeks, at doses corresponding to calculated daily doses of 0, 1, 10, 100 and 1000ngTCDD/kgbw (H/W only). Femur, tibia and vertebra from the L-E and H/W rats were analyzed by peripheral quantitative computed tomography (pQCT) and biomechanical testing at multiple sites. Dose-response modeling was performed to establish benchmark doses for the analyzed bone parameters, and to quantify strain sensitivity differences for those parameters, which were affected by TCDD exposure in both rat strains.
Bone geometry and bone biomechanical parameters were affected by TCDD exposure, while bone mineral density parameters were less affected. The trabecular area at proximal tibia and the endocortical circumference at tibial diaphysis were the parameters that showed the highest maximal responses. Significant strain differences in response to TCDD treatment were observed, with the L-E rat being the most sensitive strain. For the parameters that were affected in both strains, the differences in sensitivity were quantified, showing the most pronounced (about 49-fold) strain difference for cross-sectional area of proximal tibia.
The study provides novel information about TCDD-induced bone alterations at doses, which are of relevance from a health risk assessment point of view. In addition, the obtained results provide further support for a distinct role of the AhR in TCDD-induced bone alterations, and suggest that the benchmark dose modeling approach is appropriate for quantitative evaluation of bone toxicity parameters.
[show abstract][hide abstract] ABSTRACT: In this study, differences in sensitivity between Long-Evans (L-E; dioxin sensitive) and Han/Wistar (H/W; dioxin resistant) rats following long-term exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) were statistically and quantitatively investigated. Sensitivity differences were analyzed by comparing benchmark doses (BMDs) for the two strains considering a number of toxicological endpoints including data on body and organ weights, hepatic foci, hepatic CYP1A1 induction, as well as tissue retinoid levels. Dose-response relationships for L-E and H/W rats, described by the Hill function, were assumed to be parallel, which was supported according to statistical analysis. It was concluded that L-E and H/W rats differed statistically in their response to TCDD treatment for most of the parameters investigated. Differences between the strains were most pronounced for hepatic foci; L-E rats were approximately 20-40 times more sensitive than H/W rats. For body and organ weight parameters, L-E rats were approximately 10-20 times more sensitive than H/W rats. For retinoid parameters and hepatic CYP1A1 induction, estimated differences between the strains were generally about 5-fold, and associated with a low uncertainty. In conclusion, the present study employs a dose-response modeling approach suitable for statistical evaluation of strain and species differences in sensitivity to chemical exposure. The study demonstrates quantitatively the differences in sensitivity between the L-E and H/W rat strains following long-term TCDD exposure.
Regulatory Toxicology and Pharmacology 02/2010; 57(2-3):136-45. · 2.13 Impact Factor
[show abstract][hide abstract] ABSTRACT: The emission-exposure and exposure-response (toxicity) relationships are different for different emission source categories of anthropogenic primary fine particulate matter (PM2.5). These variations have a potentially crucial importance in the integrated assessment, when determining cost-effective abatement strategies. We studied the importance of these variations by conducting a sensitivity analysis for an integrated assessment model. The model was developed to estimate the adverse health effects to the Finnish population attributable to primary PM2.5 emissions from the whole of Europe. The primary PM2.5 emissions in the whole of Europe and in more detail in Finland were evaluated using the inventory of the European Monitoring and Evaluation Programme (EMEP) and the Finnish Regional Emission Scenario model (FRES), respectively. The emission-exposure relationships for different primary PM2.5 emission source categories in Finland have been previously evaluated and these values incorporated as intake fractions into the integrated assessment model. The primary PM2.5 exposure-response functions and toxicity differences for the pollution originating from different source categories were estimated in an expert elicitation study performed by six European experts on air pollution health effects. The primary PM2.5 emissions from Finnish and other European sources were estimated for the population of Finland in 2000 to be responsible for 209 (mean, 95% confidence interval 6–739) and 357 (mean, 95% CI 8–1482) premature deaths, respectively. The inclusion of emission-exposure and toxicity variation into the model increased the predicted relative importance of traffic related primary PM2.5 emissions and correspondingly, decreased the predicted relative importance of other emission source categories. We conclude that the variations of emission-exposure relationship and toxicity between various source categories had significant impacts for the assessment on premature deaths caused by primary PM2.5.
[show abstract][hide abstract] ABSTRACT: The intake fraction (iF) has been defined as the integrated incremental intake of a pollutant released from a source category or region summed over all exposed individuals. In this study we evaluated the iFs in the population of Europe for emissions of anthropogenic primary fine particulate matter (PM2.5) from sources in Europe, with a more detailed analysis of the iF from Finnish sources. Parameters for calculating the iFs include the emission strengths, the predicted atmospheric concentrations, European population data, and the average breathing rate per person. Emissions for the whole of Europe and Finland were based on the inventories of the European Monitoring and Evaluation Programme (EMEP) and the Finnish Regional Emission Scenario (FRES) model, respectively. The atmospheric dispersion of primary PM2.5 was computed using the regional-scale dispersion model SILAM. The iFs from Finnish sources were also computed separately for six emission source categories. The iFs corresponding to the primary PM2.5 emissions from the European countries for the whole population of Europe were generally highest for the densely populated Western European countries, second highest for the Eastern and Southern European countries, and lowest for the Northern European and Baltic countries. For the entire European population, the iF values varied from the lowest value of 0.31 per million for emissions from Cyprus, to the highest value of 4.42 per million for emissions from Belgium. These results depend on the regional distribution of the population and the prevailing long-term meteorological conditions. Regarding Finnish primary PM2.5 emissions, the iF was highest for traffic emissions (0.68 per million) and lowest for major power plant emissions (0.50 per million). The results provide new information that can be used to find the most cost-efficient emission abatement strategies and policies.
[show abstract][hide abstract] ABSTRACT: We introduce a simple concept called Population-based Time-Average Inhalation (PTAI) intended to evaluate the relative effect of emission sources on population exposure. The PTAI is defined as the sum of the individual time-average inhalations at a particular distance from an air pollution source. We demonstrate this concept by evaluating the PTAI's for primary fine particulate matter emission from vehicular traffic and domestic wood combustion in Finland. The PTAI's for these two pollution categories were evaluated by combining the emission volume and location data with population location data and with the time-average inhalation per person. The PTAI for the vehicular traffic was significantly higher than that for domestic wood combustion. The result suggests that there is a difference in the exposure potency (per emission volume) between these two sources. The PTAI differences between domestic wood combustion sub-sectors imply that there is a significant difference also in exposure potency between different sub-sectors.
Boreal Environment Research 01/2009; 14(5):850-860. · 1.75 Impact Factor
[show abstract][hide abstract] ABSTRACT: Dioxins exert their major toxicologic effects by binding to the aryl hydrocarbon receptor (AHR) and altering gene transcription.
Numerous dioxin-responsive genes previously were identified both by conventional biochemical and molecular techniques and
by recent mRNA expression microarray studies. However, of the large set of dioxin-responsive genes the specific genes whose
dysregulation leads to death remain unknown. To identify specific genes that may be involved in dioxin lethality we compared
changes in liver mRNA levels following exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in three strains/lines of dioxin-sensitive rats with changes in three dioxin-resistant rat strains/lines. The
three dioxin-resistant strains/lines all harbor a large deletion in the transactivation domain of the aryl hydrocarbon receptor
(AHR). Despite this deletion, many genes exhibited a “Type-I” response—that is, their responses were similar in dioxin-sensitive
and dioxin-resistant rats. Several genes that previously were well established as being dioxin-responsive or under AHR regulation
emerged as Type-I responses (e.g. CYP1A1, CYP1A2, CYP1B1 and Gsta3). In contrast, a relatively small number of genes exhibited
a Type-II response—defined as a difference in responsiveness between dioxin-sensitive and dioxin-resistant rat strains. Type-II
genes include: malic enzyme 1, ubiquitin C, cathepsin L, S-adenosylhomocysteine hydrolase and ferritin light chain 1. In silico searches revealed that AH response elements are conserved
in the 5′-flanking regions of several genes that respond to TCDD in both the Type-I and Type-II categories. The vast majority
of changes in mRNA levels in response to 100 μg/kg TCDD were strain-specific; over 75% of the dioxin-responsive clones were
affected in only one of the six strains/lines. Selected genes were assessed by quantitative RT-PCR in dose-response and time-course
experiments and responses of some genes were assessed in Ahr-null mice to determine if their response was AHR-dependent. Type-II genes may lie in pathways that are central to the difference
in susceptibility to TCDD lethality in this animal model.
Archives of Toxicology 12/2008; 82(11):831. · 5.22 Impact Factor
[show abstract][hide abstract] ABSTRACT: Full text available at http://urn.fi/URN:NBN:fi-fe201204193249
Juha Pekkanen, Matti Jantunen, Raimo Pohjanvirta, Raimo O. Salonen, Jouni T.
Tuomisto, Matti Viluksela, Jouko Tuomisto
Centre for environmental health risk analysis 2002-2007. Final report for the Finnish
Programme for Centres of Excellence in Research
Publications of the National Public Health Institute, B20/2008, 58 Pages
ISBN 978-951-740-797-7; 978-951-740-79 (pdf -version)
ISSN 0359-3576, http://www.ktl.fi/ portal/2920
General objective of the Centre for Environmental Health Risk Analysis was to improve
environmental health risk analysis by increasing the understanding of environmental
risks at all levels from molecular mechanisms to societal needs. This required both highquality
research and better methods of risk characterization.
For both dioxin and urban air particulate pollution (PM), the present risk
assessment practices do not optimally benefit human health. Fish may contain toxicants,
but its nutrients are beneficial for health. Risk assessors and authorities have
recommended restrictions to fish consumption, even if the net effect on health is
negative. We calculated that by reducing salmon consumption in Europe, one might
cause 100-fold more loss than saving of life. Current urban exposures to PM are
calculated to cause 350 000 premature deaths annually in Europe while cancers due to
urban air metals (As, Cd, Ni) are by far fewer and more uncertain. Still the carcinogenic
metals are strictly regulated on the basis of occupational data and experimental animal
data, but there is little legislative effort to effectively reduce current PM exposures.
Effective risk assessment requires a thorough knowledge of the full causal chain
leading to health effects. Own scientific research is needed to be able to interpret and to
fill in the gaps in the available information. The Centre’s work focused on developing
innovative methods for assessment of exposure and for doing risk analysis, on
understanding the mechanisms of adverse effects through toxicological, molecular
biology, and human studies, and on multidisciplinary collaboration between exposure
scientists, toxicologists, epidemiologists, and risk analysts both in field works and in
risk analysis. Internationally important and relevant scientific results were achieved for
both dioxin and PM.
In all of these areas international and domestic collaboration with high-standard
scientific institutes has been crucial, and we have been able to establish permanent
networks that will be highly important also after this project has ended.
Keywords: Air pollution, fine particles, ultrafine particles, coarse particles, exposure,
epidemiology, toxicology, dioxins, TCDD, developmental toxicity, teeth, risk analysis, risk
assessment, open risk assessment
Publications of the National Public Health Institute. 10/2008; B20(1-2).
[show abstract][hide abstract] ABSTRACT: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) causes hepatic accumulation of biliverdin and its monoglucuronide in moderately TCDD-resistant line B rats, but not in highly TCDD-resistant line A rats. In the mammalian heme degradation process, heme is cleaved to biliverdin by the rate-limiting enzyme heme oxygenase-1 (HO-1). Subsequently, biliverdin IXalpha reductase (BVRA) catalyzes the reduction of biliverdin to bilirubin. In heme biosynthesis, the rate-limiting enzyme is delta-aminolevulinic acid synthetase 1 (ALAS1). The effect of TCDD on HO-1, BVRA and ALAS1 was studied at the levels of mRNA (all three enzymes), protein expression (HO-1), and enzymatic activity (BVRA, liver only) in order to determine whether the accumulation of biliverdin could be due to their altered expression. In both lines A and B, 300 microg/kg TCDD transiently repressed hepatic HO-1 mRNA on day 2 but induced HO-1 protein expression at later time-points; however, the impact emerged earlier (day 14 vs. day 35) in line B rats. In spleen, TCDD repressed HO-1 mRNA and protein expression in lines A and B through days 2-35, but did not affect its mRNA levels in TCDD-sensitive L-E rats (10 days after 100 microg/kg). In all rat strains/lines, there was a strong repression of ALAS1 and a moderate induction of BVRA mRNA in liver, but mostly not in spleen. Hepatic BVRA activity was increased in lines A and B on day 14. At 5 weeks, it was still elevated in line A but reduced to 51% of control in line B. The results suggest that hepatic heme degradation is induced by TCDD in rats; however, this does not alone explain the accumulation of biliverdin in line B rats. Other factors such as the late repression of BVRA found here and possibly oxidative stress may be important contributors to biliverdin accumulation in these rats.
[show abstract][hide abstract] ABSTRACT: Dioxins exert their major toxicologic effects by binding to the aryl hydrocarbon receptor (AHR) and altering gene transcription. Numerous dioxin-responsive genes previously were identified both by conventional biochemical and molecular techniques and by recent mRNA expression microarray studies. However, of the large set of dioxin-responsive genes the specific genes whose dysregulation leads to death remain unknown. To identify specific genes that may be involved in dioxin lethality we compared changes in liver mRNA levels following exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in three strains/lines of dioxin-sensitive rats with changes in three dioxin-resistant rat strains/lines. The three dioxin-resistant strains/lines all harbor a large deletion in the transactivation domain of the aryl hydrocarbon receptor (AHR). Despite this deletion, many genes exhibited a "Type-I" response-that is, their responses were similar in dioxin-sensitive and dioxin-resistant rats. Several genes that previously were well established as being dioxin-responsive or under AHR regulation emerged as Type-I responses (e.g. CYP1A1, CYP1A2, CYP1B1 and Gsta3). In contrast, a relatively small number of genes exhibited a Type-II response-defined as a difference in responsiveness between dioxin-sensitive and dioxin-resistant rat strains. Type-II genes include: malic enzyme 1, ubiquitin C, cathepsin L, S-adenosylhomocysteine hydrolase and ferritin light chain 1. In silico searches revealed that AH response elements are conserved in the 5'-flanking regions of several genes that respond to TCDD in both the Type-I and Type-II categories. The vast majority of changes in mRNA levels in response to 100 microg/kg TCDD were strain-specific; over 75% of the dioxin-responsive clones were affected in only one of the six strains/lines. Selected genes were assessed by quantitative RT-PCR in dose-response and time-course experiments and responses of some genes were assessed in Ahr-null mice to determine if their response was AHR-dependent. Type-II genes may lie in pathways that are central to the difference in susceptibility to TCDD lethality in this animal model.
Archives of Toxicology 06/2008; 82(11):809-30. · 5.22 Impact Factor
[show abstract][hide abstract] ABSTRACT: The authors have performed a structured expert judgement study of the population mortality effects of fine particulate matter (PM2.5) air pollution. The, opinions of six European air pollution experts were elicited. The ability of each expert to probabilistically characterize uncertainty was evaluated using 12 calibration questions-relevant variables whose true values were unknown at the time of elicitation, but available at the time of analysis. The elicited opinions exhibited both uncertainty and disagreement. It emerged that there were significant differences in expert performance. Two combinations of the experts' judgements were computed and evaluated-one in which each expert's views received equal weight; the other in which the expert's judgements were weighted by their performance on the calibration variables. When the performance of these combinations was evaluated the equal-weight combination exhibited acceptable performance, but was nonetheless inferior to the performance-based combination. In general, the experts agreed with published studies for the best estimate of all-cause mortality from PM2.5; however, as would be expected, they gave confidence intervals that were several times broader than the statistical confidence intervals taken directly from the most frequently cited published studies. The experts were rather comfortable with applying epidemiological results from one geographic region to another. However, there was more uncertainty and disagreement about issues of timing of the effect and about the relative toxicity of different constituents of PM2.5. Even so, the experts were in fairly good agreement that an appreciable fraction of the long-term health effects occurs within a few months after the exposure and that combustion-derived particles are more toxic than PM2.5 on average, while secondary sulphates, nitrates and/or crustal materials may be less toxic. These assessments bring very valuable and relevant information to air pollution risk assessment. (c) 2007 Elsevier Ltd. All rights reserved.
[show abstract][hide abstract] ABSTRACT: Dioxins and airborne fine particles are both environmental health problems that have been the subject of active public debate. Knowledge on fine particles has increased substantially during the last 10 years, and even the current, lowered levels in the Europe and in the United States appear to be a major public health problem. On the other hand, dioxins are ubiquitous persistent contaminants, some being carcinogens at high doses, and therefore of great concern. Our aim was to (a) quantitatively analyze the two pollutant health risks and (b) study the changes in risk in view of the current and forthcoming EU legislations on pollutants. We performed a comparative risk assessment for both pollutants in the Helsinki metropolitan area (Finland) and estimated the health effects with several scenarios. For primary fine particles: a comparison between the present emission situation for heavy-duty vehicles and the new fine particle emission standards set by the EU. For dioxins: an EU directive that regulates commercial fishing of Baltic salmon and herring that exceed the dioxin concentration limit set for fish meat, and a derogation (= exemption) from the directive for these two species. Both of these two decisions are very topical issues and this study estimates the expected changes in health effects due to these regulations. It was found that the estimated fine particle risk clearly outweighed the estimated dioxin risk. A substantial improvement to public health could be achieved by initiating reductions in emission standards; about 30 avoided premature deaths annually in the study area. In addition, the benefits of fish consumption due to omega-3 exposure were notably higher than the potential dioxin cancer risk. Both regulations were instigated as ways of promoting public health.
[show abstract][hide abstract] ABSTRACT: Primary fine particulate matter (PM2.5) emissions from low-altitude sources, such as traffic and domestic combustion, may cause immediate exposure near the source. In this paper we present emission estimate and uncertainty analysis of PM2.5 emissions from the vehicular traffic and domestic wood combustion sectors. Our estimate of national PM2.5 emissions in 2000 from domestic wood combustion was 7.6 Gg a(-1) and that from vehicular traffic, including non-exhaust emissions, 5.8 Gg a(-1). These values correspond to 25% and 19% of the national total PM 2.5 emissions, respectively. The uncertainties were high for non-exhaust traffic and domestic wood combustion emissions, 37% down, 53% up and 36% down, 50% up of the mean value (95% confidence interval limits), respectively. For traffic exhaust emissions, the uncertainties were lower, 11% down, 13% up. Uncertainties in the domestic combustion emission factors were the most important individual parameters accounting for total uncertainty.
Boreal Environment Research 01/2008; 13(5):465-474. · 1.75 Impact Factor
[show abstract][hide abstract] ABSTRACT: Polybrominated diphenyl ethers (PBDEs) are widely used in Western countries.
Because the prevalence of cryptorchidism appears to be increasing, we investigated whether exposure to PBDEs was associated with testicular maldescent.
In a prospective Danish-Finnish study, 1997-2001, all boys were examined for cryptorchidism. We analyzed whole placentas (for 95 cryptorchid/185 healthy boys) and individual breast milk samples (62/68) for 14 PBDEs and infant serum samples for gonadotropins, sex-hormone binding globulin, testosterone, and inhibin B.
In 86 placenta-milk pairs, placenta PBDE concentrations in fat were lower than in breast milk, and a larger number of congeners were nondetectable. There was no significant difference between boys with and without cryptorchidism for individual congeners, the sum of 5 most prevalent, or all 14 congeners. The concentration of PBDEs in breast milk was significantly higher in boys with cryptorchidism than in controls (sum of BDEs 47, 153, 99, 100, 28, 66, and 154: median, 4.16 vs. 3.16 ng/g fat; p < 0.007). There was a positive correlation between the sum of PBDEs and serum luteinizing hormone (p < 0.033). The sum of PBDEs in breast milk did not differ between Denmark and Finland (median, 3.52 vs. 3.44 ng/g fat), but significant differences in some individual congeners were found.
Two different proxies were used for prenatal PBDE exposure, and levels in breast milk, but not in placenta, showed an association with congenital cryptorchidism. Other environmental factors may contribute to cryptorchidism. Our observations are of concern because human exposure to PBDEs is high in some geographic areas.
Environmental Health Perspectives 11/2007; 115(10):1519-26. · 7.26 Impact Factor