A systematic review of cancer risk among users of smokeless tobacco (Swedish snus) exclusively, compared with no use of tobacco.

The main objective of this systematic review was to assess cancer risk, and mortality after cancer diagnosis, for exclusive users of Swedish snus, compared with non-users of tobacco. We followed international standards for systematic reviews and graded our confidence in the risk estimates using the GRADE approach. Our search gave 2450 articles, of which 67 were assessed in full text against our inclusion criteria. Of these, 14 cohort-studies and one case-control study were included in the review. The studies investigated risk of cancer in the oral cavity or oropharynx (3 studies), esophagus (1 study), stomach (1 study), pancreas (2 studies), colorectum (2 studies), anus (1 study) and lung (1 study), as well as malignant lymphoma (1 study), leukemia and multiple myeloma (1 study), melanoma (1 study), any cancer (1 study) and mortality after cancer diagnosis (4 studies). Cancer risk could only be evaluated in men as there was a general lack of data for women. All included studies were evaluated to have a moderate risk of bias, mostly related to validity of exposure information. An increased risk of cancer of the esophagus, pancreas, stomach and rectum as well as an association between use of snus and increased mortality after a cancer diagnosis was reported. Our confidence in the various risk estimates varied from moderate through low to very low.

Factors associated with initiation and use of snus among adolescents.

AIM: We investigated factors associated with the initiation and continuation of snus use in adolescents in Norway. The associations with adolescents' own educational plans, the parents' educational level(s) and tobacco habits were estimated. METHODS: In this cross-sectional questionnaire-based study, 1465 patients aged 18-20 years participated. The questionnaire was administered at regular dental examinations in the public dental health service. To assess the association between individual factors and the initiation of tobacco habits, a generalised structural equation model with random effects at the clinic level was used. Binary responses were modelled using multilevel binary logistic regression, while the number of snus boxes used per month was modelled using a multilevel Poisson regression model. RESULTS: Of current (daily and occasional) tobacco users, 85% were snus users, including dual users of both snus and cigarettes. The median age of snus initiation was 16 years. Both parental snus use and smoking were associated with an increased risk of snus initiation, snus use and a higher amount of use. An increased risk of using snus was associated with male gender and with no educational plans or planning for further vocational education. The amount of snus used was higher among current snus users with a prior smoking history and among those planning for further vocational education. CONCLUSIONS: These findings may aid in developing and targeting tobacco prevention strategies aimed at young people. Tobacco prevention measures should start at the elementary school level. The strong association with parental tobacco habits underlines the importance of parents' influence on their children's tobacco use.

Oral lesions associated with daily use of snus, a moist smokeless tobacco product. A cross-sectional study among Norwegian adolescents.

OBJECTIVE: Use of snus, a moist, smokeless tobacco product, may lead to local changes in the oral mucous membrane in the area where the snus is placed. It can also cause irreversible gingival retraction. This cross-sectional study aimed to investigate the relationship between use of snus, oral mucosal lesions (snus induced lesions) and gingival retractions among adolescents in Norway. MATERIAL AND METHODS: All 18-20 years olds visiting public dental health clinics in the south-eastern region of Norway between October 2015 and December 2016 were invited to participate. All participants (n = 1363) filled in an electronic questionnaire before a clinical examination. Of these, 216 used snus daily. RESULTS: Snus induced lesions were observed in 79.2% of daily snus using participants. In adjusted regression analyses, the odds of having a more severe lesion as opposed to a less severe lesion were 1.12 times greater for each additional box of snus used in a month (p < .01). Women were 46% less likely to have a severe lesion than men (p = .03). Gingival retractions were observed in 18.4% of the participants. The odds for dental retraction were significantly higher by 34% for each year of snus use. CONCLUSIONS: Most of the adolescents using snus had snus induced lesions, whereas approximately one-fifth had gingival retractions. The severity of the lesion and gingival retraction increased with the amount of snus boxes used and the duration of the snus use, respectively.

TEGDMA and filler particles from dental composites additively attenuate LPS-induced cytokine release from the macrophage cell line RAW 264.7.

OBJECTIVES: Due to incomplete curing and material degradation, cells in the oral cavity may be exposed to monomers and filler particles from dental composite fillings. The objective of the present study was to investigate if combined exposures to particles and a methacrylate monomer from composite fillings resulted in additive effects on the macrophage immune response. MATERIAL AND METHODS: Two filler particles, Nanosilica (12 nm) and Quartz (1 µm), were studied at concentrations 0.5-4 µg/cm(2), while the methacrylate monomer triethyleneglycol dimethacrylate (TEGDMA) was applied at 5 and 50 µM. RAW 264.7 macrophages were exposed to monomers and/or particles for 24 h, with a subsequent 24 h combined exposure to monomers and/or particles and the bacterial factor lipopolysaccharide (LPS) to stimulate an immune response. Release of the pro-inflammatory cytokines interleukin-1ß (IL-1ß) and tumor necrosis factor-α (TNF-α) were measured as well as the cellular viability. RESULTS: Co-exposure to Nanosilica and Quartz resulted in an additive attenuation of the LPS-induced IL-1ß release. Moreover, co-exposure to TEGDMA and both types of filler particles also resulted in an additive attenuation, although with a weak synergistic trend. The cellular viability and TNF-α release were not significantly affected by the exposures. CONCLUSION: The present findings emphasize the necessity of considering effects of combined exposure to dental degradation products in future risk assessments. CLINICAL RELEVANCE: Attenuated cytokine release could have implications for the macrophage immune response and result in impaired bacterial clearance. Further studies are necessary to determine implications for formation of dental biofilms and caries development.

Are the health risks of moist oral snuff (snus) underestimated? / Er helserisikoen ved snus undervurdert?

The use of moist oral snuff (snus) has increased significantly, particularly among young adults who have not previously smoked. Snus increases the risk of cancer, cardiovascular disease, type-2 diabetes and birth defects.

AhR and Arnt differentially regulate NF-κB signaling and chemokine responses in human bronchial epithelial cells.

BACKGROUND: The aryl hydrocarbon receptor (AhR) has gradually emerged as a regulator of inflammation in the lung and other tissues. AhR may interact with the p65-subunit of the nuclear factor (NF)-κB transcription factors, but reported outcomes of AhR/NF-κB-interactions are conflicting. Some studies suggest that AhR possess pro-inflammatory activities while others suggest that AhR may be anti-inflammatory. The present study explored the impact of AhR and its binding partner AhR nuclear translocator (Arnt) on p65-activation and two differentially regulated chemokines, CXCL8 (IL-8) and CCL5 (RANTES), in human bronchial epithelial cells (BEAS-2B). RESULTS: Cells were exposed to CXCL8- and CCL5-inducing chemicals, 1-nitropyrene (1-NP) and 1-aminopyrene (1-AP) respectively, or the synthetic double-stranded RNA analogue, polyinosinic-polycytidylic acid (Poly I:C) which induced both chemokines. Only CXCL8, and not CCL5, appeared to be p65-dependent. Yet, constitutively active unligated AhR suppressed both CXCL8 and CCL5, as shown by siRNA knock-down and the AhR antagonist α-naphthoflavone. Moreover, AhR suppressed activation of p65 by TNF-α and Poly I:C as assessed by luciferase-assay and p65-phosphorylation at serine 536, without affecting basal p65-activity. In contrast, Arnt suppressed only CXCL8, but did not prevent the p65-activation directly. However, Arnt suppressed expression of the NF-κB-subunit RelB which is under transcriptional regulation by p65. Furthermore, AhR-ligands alone at high concentrations induced a moderate CXCL8-response, without affecting CCL5, but suppressed both CXCL8 and CCL5-responses by Poly I:C. CONCLUSION: AhR and Arnt may differentially and independently regulate chemokine-responses induced by both inhaled pollutants and pulmonary infections. Constitutively active, unligated AhR suppressed the activation of p65, while Arnt may possibly interfere with the action of activated p65. Moreover, ligand-activated AhR suppressed CXCL8 and CCL5 responses by other agents, but AhR ligands alone induced CXCL8 responses when given at sufficiently high concentrations, thus underscoring the duality of AhR in regulation of inflammation. We propose that AhR-signaling may be a weak activator of p65-signaling that suppresses p65-activity induced by strong activators of NF-κB, but that its anti-inflammatory properties also are due to interference with additional pathways.

Long-term bisphenol A exposure accelerates insulitis development in diabetes-prone NOD mice.

Exposure to the endocrine disruptor (ED) bisphenol A (BPA) used in polycarbonate plastic and epoxy resins appears ubiquitous since BPA can be found in over 90% of analyzed urine samples from all age groups. There is a parallel occurrence of increased prevalence in type 1 diabetes mellitus (T1DM) and an increased exposure to EDs the last decades. T1DM is caused by insulin deficiency due to autoimmune destruction of insulin producing pancreatic beta cells and has been suggested to be induced by various environmental factors acting together with a genetic predisposition. The objective of the present study was to investigate the effect of BPA (0, 1 and 100 mg/l BPA in the drinking water) on T1DM development in nonobese diabetic (NOD) mice, spontaneously developing T1DM. Histological evaluation of pancreas from 12-weeks-old female mice revealed significantly increased insulitis in mice exposed to 1 mg/l BPA, while the insulitis was less severe at the higher BPA exposure. Serum glucose levels in the 1 mg/ml BPA group tended to be hyperglycaemic, also indicating an accelerated onset of T1DM. The high BPA exposure seemed to counteract the diabetes development in females and also in male NOD mice for both BPA concentrations. Prior to insulitis, both BPA concentrations resulted in increased apoptosis and reduced numbers of tissue resident macrophages in pancreatic islets. In conclusion, long-term BPA exposure at a dose three times higher than the tolerable daily intake of 50 µg/kg, appeared to accelerate spontaneous insulitis and diabetes development in NOD mice.

Silver release from dentine treated with combinations of silver diamine fluoride, potassium iodide and etching.

For individuals with very high to extremely high caries activity and poor control of daily oral hygiene, a simple treatment for arresting their caries activity is necessary. Silver Diamine Fluoride (SDF) has become increasingly common for this purpose due to its efficacy and ease of application. To avoid or reduce tooth discoloration after SDF treatment potassium iodide (KI) may be applied. However, the release of silver from SDF-treated tooth surfaces may be of concern. Thus, the aim of the present study was to quantify the amount of silver leached in both a short- and long-term perspective. In this in vitro experiment we measured the cumulative release of silver from SDF-treated dentin surfaces with and without imminent application of KI, and with and without phosphoric acid etching as pre-treatment, after 24 h and weekly for four weeks. The release of silver was highest after 24 h for all treatment groups, with a significant drop after this point. When etching was not used, the use of KI did not affect the release of silver. However, when etching was used, there was a significantly lower silver release when KI was also used compared to when KI was not used. This effect was largest for the first two weeks, after which the difference was smaller as all groups released low amounts of silver.

Use of Swedish smokeless tobacco during pregnancy: A systematic review of pregnancy and early life health risk.

BACKGROUND AND AIMS: Smokeless tobacco is a heterogeneous product group with diverse composition and prevalence globally. Tobacco use during pregnancy is concerning due to the risk of adverse pregnancy outcomes and effects on child health. Nicotine may mediate several of these effects. This systematic review measured health outcomes from Swedish smokeless tobacco (snus) use during pregnancy. METHOD: Literature search was conducted by an information specialist in May 2022. We included human studies of snus use during pregnancy compared with no tobacco use, assessed risk of bias, conducted a meta-analysis and assessed confidence in effect-estimates using Grading of Recommendations, Assessment, Development and Evaluations (GRADE). RESULTS: We included 18 cohort studies (42 to 1 006 398 participants). Snus use during pregnancy probably (moderate confidence in risk estimates) increase the risk of neonatal apnea, adjusted odds ratio 95% confidence interval [aOR (95% CI)] 1.96 (1.30 to 2.96). Snus use during pregnancy possibly (low confidence in risk estimates) increase the risk of stillbirths aOR 1.43 (1.02 to 1.99), extremely premature births aOR 1.69 (1.17 to 2.45), moderately premature birth aOR 1.26 (1.15 to 1.38), SGA aOR 1.26 (1.09 to 1.46), reduced birth weight mean difference of 72.47 g (110.58 g to 34.35 g reduction) and oral cleft malformations aOR 1.48 (1.00 to 2.21). It is uncertain (low confidence in risk estimates, CI crossing 1) whether snus use during pregnancy affects risk of preeclampsia aOR 1.11 (0.97 to 1.28), antenatal bleeding aOR 1.15 (0.92 to 1.44) and very premature birth aOR 1.26 (0.95 to 1.66). Risk of early neonatal mortality and altered heart rate variability is uncertain, very low confidence. Snus using mothers had increased prevalence of caesarean sections, low confidence. CONCLUSIONS: This systematic review reveals that use of smokeless tobacco (snus) during pregnancy may adversely impact the developing child.

Polycyclic aromatic hydrocarbons (PAHs) may explain the paradoxical effects of cigarette use on preeclampsia (PE).

Tobacco smoking and use of snus (smokeless tobacco) are associated with adverse effects on pregnancy and neonatal outcomes. Nicotine is considered a key toxicant involved in effects caused by both smoking and snus, while pyrolysis products including polycyclic aromatic hydrocarbons (PAHs) in cigarette smoke represents the constituents most unequally divided between these two groups of tobacco products. The aim of this review was: i) to compare the impact, in terms of relative effect estimates, of cigarette smoking and use of Swedish snus on pregnancy outcomes using similar non-tobacco user controls, and ii) to examine whether exposure to PAHs from smoking could explain possible differences in impact on pregnancy outcomes. We systematically searched MEDLINE, Embase, PsycInfo, Web of Science and the Cochrane Database of Systematic Reviews up to October 2021 and identified studies reporting risks for adverse pregnancy and neonatal outcomes associated with snus use and with smoking relative to pregnant women with no use of tobacco. Both snus use and smoking were associated with increased risk of stillbirth, preterm birth, and oral cleft malformation, with comparable point estimates. These effects were likely due to comparable nicotine exposure. We also found striking differences. While both smoking and snus increased the risk of having small for gestational age (SGA) infants, risk from maternal smoking was markedly higher as was the reduction in birthweight. In contrast, the risk of preeclampsia (PE) was markedly lower in smokers than in controls, while snus use was associated with a slightly increased risk. We suggest that PAHs acting via AhR may explain the stronger effects of tobacco smoking on SGA and also to the apparent protective effect of cigarette smoking on PE. Possible mechanisms involved include: i) disrupted endocrine control of fetal development as well as placental development and function, and ii) stress adaption and immune suppression in placenta and mother.

Mono(2-ethylhexyl) phthalate induces both pro- and anti-inflammatory responses in rat alveolar macrophages through crosstalk between p38, the lipoxygenase pathway and PPARalpha.

Airway inflammation is important in asthma pathogenesis. Recent epidemiological data have indicated an association between asthma symptoms in children and exposure to di(2-ethylhexyl) phthalate (DEHP). Thus, we have studied inflammatory responses in primary rat alveolar macrophages (AMs) after exposure to mono(2-ethylhexyl) phthalate (MEHP), the major primary metabolite of DEHP. First, we show that MEHP induces a dose-dependent release of the pro-inflammatory tumour necrosis factor-alpha (TNF-alpha) in AMs, giving a maximal (5-fold) increase at 0.7 mM. This concentration also induced some cell death. MEHP also induced phosphorylation of MAPK p38, while the p38 inhibitor SB 202190 reduced MEHP-induced TNF-alpha, suggesting a p38-dependent cytokine production. Next, we elucidated possible effects of MEHP on the 5-lipoxygenase (5-LO) pathway and found that MEHP caused increased leukotriene (LTB(4)) release. Further, we found that the 5-LO inhibitor nordihydrogualaretic acid (NDGA) significantly reduced both MEHP-induced TNF-alpha release and MEHP-induced formation of reactive oxygen species (ROS), supporting an involvement of the 5-LO pathway in MEHP induced inflammatory reactions. Last, we found that MK-886, a known inhibitor of peroxisome proliferator-activated receptor alpha (PPARalpha), increased the MEHP-induced TNF-alpha response. This indicates that MEPH-PPARalpha binding mediates an anti-inflammatory signal.

Phthalate exposure and allergic diseases: Review of epidemiological and experimental evidence.

Phthalates are among the most ubiquitous environmental contaminants and endocrine-disrupting chemicals. Exposure to phthalates and related health effects have been extensively studied over the past four decades. An association between phthalate exposure and allergic diseases has been suggested, although the literature is far from conclusive. This article reviews and evaluates epidemiological (n = 43), animal (n = 49), and cell culture studies (n = 42), published until the end of 2019, on phthalates and allergic diseases, such as asthma, rhinoconjunctivitis, and eczema. In contrast to earlier reviews, emphasis is placed on experimental studies that use concentrations with relevance for human exposure. Epidemiological studies provide support for associations between phthalate exposures and airway, nasal, ocular, and dermal allergic disease outcomes, although the reported significant associations tend to be weak and demonstrate inconsistencies for any given phthalate. Rodent studies support that phthalates may act as adjuvants at levels likely to be relevant for environmental exposures, inducing respiratory and inflammatory effects in the presence of an allergen. Cell culture studies demonstrate that phthalates may alter the functionality of innate and adaptive immune cells. However, due to limitations of the applied exposure methods and models in experimental studies, including the diversity of phthalates, exposure routes, and allergic diseases considered, the support provided to the epidemiological findings is fragmented. Nevertheless, the current evidence points in the direction of concern. Further research is warranted to identify the most critical windows of exposure, the importance of exposure pathways, interactions with social factors, and the effects of co-exposure to phthalates and other environmental contaminants.

The dental monomer 2-hydroxyethyl methacrylate (HEMA) causes transcriptionally regulated adaptation partially initiated by electrophilic stress.

OBJECTIVES: Cellular responses including cell death are induced by in vitro exposure to the un-polymerized dental monomer 2-hydroxyethyl methacrylate (HEMA). Activation of the Nrf2/ARE signaling pathway has been suggested to mediate the cellular responses. Activation of this pathway may occur either indirectly through generation of increased oxidative stress or through direct binding to cysteine thiols due to the electrophilic properties of HEMA. The objective of this study was to elucidate the potential mechanism of Nrf2/ARE pathway activation after HEMA exposure. METHODS: Global gene expression was investigated after exposure of the human bronchial epithelial cell line BEAS-2B to 2mM HEMA for 4h. After exposure to 0.5, 1 or 2mM HEMA for up to 24h, western analysis was performed for selected proteins. Finally, the levels of the same proteins were determined after treatment with either the antioxidants Vitamin C, Trolox (6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid) or BSO (L-buthioninesulfoximine), an inhibitor of GSH formation. RESULTS: Several of the 25 genes with the highest increase in gene transcription are related to oxidative stress responses. Increased levels of 5 corresponding proteins (HO-1, GCLC, GCLM, NQO1 and SQSTM1) were observed. Antioxidant treatment as well as inhibition of GSH did not affect upregulation of these proteins. Thus, increased ROS or reduced GSH levels appear to be of limited importance in the observed HEMA-induced changes. SIGNIFICANCE: Knowledge of the cellular responses to HEMA is important to evaluate the safety of HEMA-containing biomaterials. The results support that HEMA activates the Nrf2-ARE transcriptional pathway directly through its electrophilic properties.

Prevention of snus use: Attitudes and activities in the Public Dental Service in the south-eastern part of Norway.

Dental health care professionals have the opportunity to play a key role in tobacco prevention and cessation among adolescents. Snus use has increased in Norway, especially in the age group 16-24, whereas there has been a decline in smoking. This study investigated attitudes and activities related to snus prevention among dental health care professionals working in the Public Dental Service (PDS) in south-eastern Norway. A web-based survey with a total of 557 dentists and dental hygienists in seven counties in Norway, with a response rate of 53.5%, was carried out in 2017. Dentists' and dental hygienists' activities regarding preventive snus use intervention were analysed using the chi-square test. Intervention was measured with a score (1-5) based on four questions. Bivariate and multivariate linear regression analyses were used to investigate the associations between the explanatory variables of attitudes/activities and the outcome intervention variable. Approximately 87% of the dentists and 58% of the dental hygienists were not familiar with the "minimum intervention method" for tobacco prevention and cessation. Dental hygienists were most active in informing and supporting their patients in prevention and cessation of snus use. The PDS is an underutilized arena for tobacco prevention and cessation among adolescents, and the intervention potential is particularly high among the dentists.

Pro-Inflammatory Responses in Human Bronchial Epithelial Cells Induced by Spores and Hyphal Fragments of Common Damp Indoor Molds.

Damp indoor environments contaminated with different mold species may contribute to the development and exacerbation of respiratory illnesses. Human bronchial epithelial BEAS-2B cells were exposed to X-ray treated spores and hyphal fragments from pure cultures of Aspergillus fumigatus, Penicillum chrysogenum, Aspergillus versicolor and Stachybotrys chartarum. Hyphal fragments of A. fumigatus and P. chrysogenum induced expression and release of the pro-inflammatory cytokine interleukin (IL)-6 and the chemokine IL-8, while none of the other hyphal preparations had effects. Hyphal fragments from A. fumigatus and P. chrysogenum also increased the expression of IL-1α, IL-1ß and tumor necrosis factor (TNF)-α, but these cytokines were not released. X-ray treated spores had little or no inflammatory potential. Attenuating Toll-like receptor (TLR)-2 by blocking antibodies strongly reduced the A. fumigatus and P. chrysogenum hyphae-induced IL-6 and IL-8 release, whereas TLR4 antagonist treatment was without effects. Untreated A. fumigatus spores formed hyphae and triggered expression of pro-inflammatory genes with similarities to the effects of hyphal fragments. In conclusion, while X-ray treated spores induced no pro-inflammatory responses, hyphal fragments of A. fumigatus and P. chrysogenum enhanced a TLR2-dependent expression and release of IL-6 and IL-8.

Di-n-butyl phthalate modifies PMA-induced macrophage differentiation of THP-1 monocytes via PPARγ.

The present study examined the effects of di-n-butyl phthalate (DBP) on phorbol myristate acetate (PMA)-induced macrophage differentiation of THP-1 monocytes, determined by morphological classification and flow cytometry. Focusing on the expression of the surface marker CD36, the potential role of peroxisome proliferator-activated receptor gamma (PPARγ) was examined using various PPARγ agonists and antagonists. As the PPARγ ligand-binding domain contains multiple ligand-binding sites (LBS), agonist and antagonists targeting the different sites were used. DBP accelerated PMA-induced morphological changes and increased expression of CD36, although to a lesser degree than the PPARγ agonists rosiglitazone and 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2). A proteomics screening revealed that DBP enhanced the expression of PPARγ-regulated proteins. During combined exposures, DBP partly attenuated the effect of rosiglitazone, an agonist binding reversibly to PPARγ's canonical LBS. In contrast, DBP increased expression of CD36 in combination with 15d-PGJ2 which binds irreversibly to the canonical LBS. Thus, DBP appears to interact with both the canonical and alternative LBS. Accordingly, the antagonist GW9662, which binds to the canonical LBS, only partly reduced the DBP-induced CD36 expression, while the dual-site antagonist SR16832 completely blocked the effects of DBP. Overall, the results show that DBP modifies PMA-induced differentiation of THP-1 cells through interaction with PPARγ.

Concentrations of selected chemicals in indoor air from Norwegian homes and schools.

Both building materials and consumer products have been identified as possible sources for potentially hazardous substances like phthalates, polychlorinated biphenyls (PCBs), organophosphorous flame retardants (OPFRs), polybrominated diphenyl ethers (PBDEs) and short chain chlorinated paraffins (SCCPs) in indoor air. Thus, indoor air has been suggested to contribute significantly to human exposure to these chemicals. There is lack of data on the occurrence of several of the aforementioned chemicals in indoor air. Therefore, indoor air (gas and particulate phase) was collected from 48 households and 6 classrooms in two counties in Norway. In both the households and schools, median levels of low molecular weight phthalates (785 ng/m3), OPFRs (55 ng/m3) and SCCPs (128 ng/m3) were up to 1000 times higher than the levels of PCBs (829 pg/m3) and PBDEs (167 pg/m3). Median concentrations of dimethyl phthalate (DMP), diethyl phthalate (DEP), di-isobutyl phthalate (DiBP) and SCCPs were 3-6 times higher in households compared to schools. The levels of OPFRs, PCBs and PBDEs were similar in households and schools. In univariate analysis, the indoor concentrations of different environmental chemicals were significantly affected by location of households (OPFRs), airing of living room (some PCBs and PBDEs), presence of upholstered chair/couch (OPFRs), pet animal hold (some PBDEs) and presence of electrical heaters (selected PCBs and PBDEs). Significant correlations were also detected for the total size of households with OPFRs, frequency of vacuuming the living room with selected PCBs and PBDEs, frequency of washing the living room with selected PCBs and the total number of TVs in the households with selected phthalates and SCCPs. Finally, intake estimates indicated that indoor air contributed more or equally to low molecular weight phthalates and SCCPs exposure compared to food consumption, whereas the contribution from indoor air was smaller than the dietary intake for the other groups of chemicals.

Do Carpets Impair Indoor Air Quality and Cause Adverse Health Outcomes: A Review.

Several earlier studies have shown the presence of more dust and allergens in carpets compared with non-carpeted floors. At the same time, adverse effects of carpeted floors on perceived indoor air quality as well as worsening of symptoms in individuals with asthma and allergies were reported. Avoiding extensive carpet use in offices, schools, kindergartens and bedrooms has therefore been recommended by several health authorities. More recently, carpet producers have argued that former assessments were obsolete and that modern rugs are unproblematic, even for those with asthma and allergies. To investigate whether the recommendation to be cautious with the use of carpets is still valid, or whether there are new data supporting that carpet flooring do not present a problem for indoor air quality and health, we have reviewed the literature on this matter. We have not found updated peer reviewed evidence that carpeted floor is unproblematic for the indoor environment. On the contrary, also more recent data support that carpets may act as a repository for pollutants which may become resuspended upon activity in the carpeted area. Also, the use of carpets is still linked to perception of reduced indoor air quality as well as adverse health effects as previously reported. To our knowledge, there are no publications that report on deposition of pollutants and adverse health outcomes associated with modern rugs. However, due to the three-dimensional structure of carpets, any carpet will to some extent act like a sink. Thus, continued caution should still be exercised when considering the use of wall-to-wall carpeted floors in schools, kindergartens and offices, as well as in children's bedrooms unless special needs indicate that carpets are preferable.

Presence and leaching of bisphenol a (BPA) from dental materials.

BPA has been reported to leach from some resin based dental restorative materials and materials used for orthodontic treatment. To confirm and update previous findings, especially in light of the new temporary lower threshold value for tolerable daily BPA intake, we have investigated the leaching of BPA from 4 composite filling materials, 3 sealants and 2 orthodontic bonding materials. The materials were either uncured and dissolved in methanol or cured. The cured materials were kept in deionized water for 24 hours or 2 weeks. Samples were subsequently analyzed by ultra-performance liquid chromatography coupled to mass spectrometry (UPLC-MS-MS). The composite filling material Tetric EvoFlow® and the fissure sealant DELTON® showed significantly higher levels of BPA leaching compared to control samples for all test conditions (uncured, 24 h leaching and 2 weeks leaching). There were no significant differences in amount of leached BPA for any of the tested materials after 24 hours compared to 2 weeks. These results show that BPA is still released from some dental materials despite the general concern about potential adverse effects of BPA. However, the amounts of BPA were relatively low and most likely represent a very small contribution to the total BPA exposure.