Perfluoroalkyl substances (PFAS) are suggested to have immunosuppressive effects; exposure in utero and in the first years of life is of special concern as fetuses and small children are highly vulnerable to toxicant exposure. The objective of this study was to investigate the effect of pre-natal exposure to PFAS on responses to pediatric vaccines and immune-related health outcomes in children up to 3 years of age. In the prospective birth-cohort BraMat, a sub-cohort of the Norwegian Mother and Child Cohort Study (MoBa), pregnant women from Oslo and Akershus, Norway, were recruited during 2007-2008. Three annual questionnaire-based follow-ups were performed. Blood samples were collected from the mothers at the time of delivery and from the children at the age of 3 years. As a measure of pre-natal exposure to PFAS, the concentrations of perfluorooctanoate (PFOA), perfluorononanoate (PFNA), perfluorohexane sulfonate (PFHxS), and perfluorooctane sulfonate (PFOS) were determined in maternal blood from 99 BraMat participants. Main outcome measures were anti-vaccine antibody levels, common infectious diseases and allergy- and asthma-related health outcomes in the children up to the age of 3 years. There was an inverse association between the level of anti-rubella antibodies in the children's serum at age 3 years and the concentrations of the four PFAS. Furthermore, there was a positive association between the maternal concentrations of PFOA and PFNA and the number of episodes of common cold for the children, and between PFOA and PFHxS and the number of episodes of gastroenteritis. No associations were found between maternal PFAS concentrations and the allergy- and asthma-related health outcomes investigated. The results indicate that pre-natal exposure to PFAS may be associated with immunosuppression in early childhood.

The adjuvant effect of particles on allergic immune responses has been shown to increase with decreasing particle size and increasing particle surface area. Like ultrafine particles, carbon nanotubes (CNTs) have nano-sized dimensions and a large relative surface area and might thus increase allergic responses. Therefore, we examined whether single-walled (sw) and multi-walled (mw) CNTs have the capacity to promote allergic responses in mice, first in an sc injection model and thereafter in an intranasal model. Balb/cA mice were exposed to three doses of swCNT, mwCNT, as well as ultrafine carbon black particles (ufCBPs, Printex90) during sensitization with the allergen ovalbumin (OVA). Five days after an OVA booster, OVA-specific IgE, IgG1, and IgG2a antibodies in serum and the numbers of inflammatory cells and cytokine levels in bronchoalveolar lavage fluid (BALF) were determined. Furthermore, ex vivo OVA-induced cytokine release from mediastinal lymph node (MLN) cells was measured. In separate experiments, differential cell counts were determined in BALF 24 h after a single intranasal exposure to the particles in the absence of allergen. We demonstrate that both swCNT and mwCNT together with OVA strongly increased serum levels of OVA-specific IgE, the number of eosinophils in BALF, and the secretion of Th2-associated cytokines in the MLN. On the other hand, only mwCNT and ufCBP with OVA increased IgG2a levels, neutrophil cell numbers, and tumor necrosis factor-alpha and monocyte chemoattractant protein-1 levels in BALF, as well as the acute influx of neutrophils after exposure to the particles alone. This study demonstrates that CNTs promote allergic responses in mice.

Type 1 diabetes mellitus (T1DM) is an autoimmune disease, where destruction of beta-cells causes insulin deficiency. The incidence of T1DM has increased in the last decades and cannot entirely be explained by genetic predisposition. Several environmental factors are suggested to promote T1DM, like early childhood enteroviral infections and nutritional factors, but the evidence is inconclusive. Prenatal and early life exposure to environmental pollutants like phthalates, bisphenol A, perfluorinated compounds, PCBs, dioxins, toxicants, and air pollutants can have negative effects on the developing immune system, resulting in asthma-like symptoms and increased susceptibility to childhood infections. In this review the associations between environmental chemical exposure and T1DM development is summarized. Although information on environmental chemicals as possible triggers for T1DM is sparse, we conclude that it is plausible that environmental chemicals can contribute to T1DM development via impaired pancreatic beta-cell and immune-cell functions and immunomodulation. Several environmental factors and chemicals could act together to trigger T1DM development in genetically susceptible individuals, possibly via hormonal or epigenetic alterations. Further observational T1DM cohort studies and animal exposure experiments are encouraged.

The purpose of this study was to investigate the fate and effects of mineral oil saturated hydrocarbons (MOSH) in female Fischer 344 rats. Animals were fed control diet or diet containing various MOSH mixtures at concentrations ranging from 40 to 4000 mg/kg feed for up to 120 days. MOSH were analysed in liver, spleen, adipose tissue and remaining carcass at different sampling times. In addition to clinical effects, liver microgranulomas, hepatic inflammation, and disruption of the immune function were the main toxicological endpoints investigated. Arthritis symptoms were specifically studied in dark agouti rats. The results indicate that accumulation of MOSH depends on the mixture tested but always occurred predominantly in the liver and to a lesser extent in adipose tissue and spleen. Strong differences exist between liver and adipose tissue in terms of accumulated hydrocarbons: whereas in adipose tissue the accumulated fraction corresponds to the most volatile part of the administered mixture, in the liver, the most volatile as well as the highest boiling part of the mixture are almost absent. Also the types of hydrocarbons differ. When exposure ceases, a significant decrease of MOSH concentration was observed in the liver, but not in adipose tissue. MOSH exposure results in a significant increase in absolute and relative liver weights, the effect being dose-related, but also dependent on the mixture tested. There were large differences in the ability of the different mixtures to induce liver granulomas. The highest incidence was observed with the mixture containing the highest proportion of n-alkanes, suggesting that this fraction could play a significant role in the development of hepatic granulomas. No effects were found on the immune function, irrespective of the mixture or the dose tested.

Reversing or aborting the increase in allergic and other immunerelated noncommunicable diseases (NCDs) in the Western world, first observed for allergic rhinitis from the 1890s, 1 requires priat, or in collaboration with (in Sweden), the 3 participating hospitals were eligible, provided sufficient language skills. Women carrying more than 2 fetuses, fetuses with severe malformations or disease and infants born prior to 35.0 weeks of GA, were excluded.All infants were randomized at birth to 1 of 4 similar sized groups: (1) no intervention; (2) skin care (oil-bath at least 5 days per week from 0.5 to 9 months of age); (3) consecutive introduction, between 3 and 4 months of age, of peanut, milk, wheat, and egg at least 4 days per week complementary to breastfeeding; or (4) both interventions. Weekly electronic diaries (2-26 weeks of age) recorded skin care, infant feeding, and symptoms of allergic diseases.Adverse events (0-12 months of age) elicited relevant investigations and treatment by direct access for the participants to the local pediatric department.Data collection (Figure 1, Table S1) includes electronic questionnaires with information of health and disease in the mother, child, and family; lifestyle; environment; stress; quality of life; diet in the mother and offspring; clinical investigations; fetal and child anthropometrics; lung function; skin barrier; allergy; and blood pressure