Perfluorinated alkylate substances (PFASs) are highly persistent and may cause immunotoxic effects. PFAS-associated attenuated antibody responses to childhood vaccines may be affected by PFAS exposures during infancy, where breastfeeding adds to PFAS exposures. Of 490 members of a Faroese birth cohort, 275 and 349 participated in clinical examinations and provided blood samples at ages 18 months and 5 years. PFAS concentrations were measured at birth and at the clinical examinations. Using information on duration of breastfeeding, serum-PFAS concentration profiles during infancy were estimated. As outcomes, serum concentrations of antibodies against tetanus and diphtheria vaccines were determined at age 5. Data from a previous cohort born eight years earlier were available for pooled analyses. Prenatal exposure showed inverse associations with the antibody concentrations five years later, with decreases by up to about 20% for each two-fold higher exposure, while associations for serum concentrations at ages 18 months and 5 years were weaker. Modeling of serum-PFAS concentration showed levels for age 18 months that were similar to those measured. Concentrations estimated for ages 3 and 6 months showed the strongest inverse associations with antibody concentrations at age 5 years, particularly for tetanus. Joint analyses showed statistically significant decreases in tetanus antibody concentrations by 19% to 29% at age 5 for each doubling of the PFAS exposure in early infancy. These findings support the notion that the developing adaptive immune system is particularly vulnerable to immunotoxicity during infancy. This vulnerability appears to be the greatest during the first 6 months after birth, where PFAS exposures are affected by breast-feeding.

OBJECTIVETo investigate the long-term association of exposure to perfluoroalkylated substances, including perfluorooctanesulfonic acid (PFOS) and perfluorooctanoic acid (PFOA), during childhood (9 years) and adolescence (15 years) on indicators of adiposity and glucose metabolism in adolescence (15 years) and young adulthood (21 years). Secondarily, we aim to clarify the degree of tracking of exposure from childhood into young adulthood. RESEARCH DESIGN AND METHODSData derived from a large multicenter prospective cohort study, in which the same participants have been observed from childhood (N = 590), during adolescence (N = 444), and into young adulthood (N = 369). Stored plasma samples were analyzed for PFOS and PFOA. Indicators of adiposity comprising body height, body weight, sum of four skinfolds, and waist circumference, as well as indicators of glucose metabolism, comprising fasting blood glucose, triglyceride, and insulin levels, b-cell function, and insulin resistance, have been collected at all study waves. Multiple linear regression was applied in order to model earlier exposure on later outcome while controlling for baseline outcome levels, sex, age, and socioeconomic factors. RESULTSChildhood exposure to PFOS was associated with indicators of adiposity at 15 years of age that are displayed in elevated BMI, skinfold thickness, and waist circumference, as well as increased skinfold thickness and waist circumference at 21 years of age. PFOA exposure in childhood was associated with decreased b-cell function at 15 years of age. We did not observe associations between exposure during adolescence and indicators of adiposity and glucose metabolism in young adulthood. CONCLUSIONSThis study found evidence for childhood exposure to PFOS and PFOA predicting adiposity at 15 and 21 years of age and impaired b-cell function at 15 years of age, respectively.

Increased PFC exposure in overweight 8- to 10-year-old children was associated with higher insulin and triglyceride concentrations. Chance findings may explain some of our results, and due to the cross-sectional design, reverse causation cannot be excluded. The findings therefore need to be confirmed in longitudinal studies.

The aim of this study was to determine whether maternal exposure to persistent perfluoroalkyl substances (PFASs) affect the capability to breastfeed. In two Faroese birth cohorts (N=1,130), concentrations of five PFASs were measured in maternal serum during pregnancy or two weeks after term. Duration of breastfeeding was assessed by questionnaire and clinical interview. In adjusted linear regression models, a doubling of maternal serum PFASs was associated with a reduction in duration of both total and exclusive breastfeeding, most pronounced for perfluorooctane sulfonic acid (PFOS) where a doubling was associated with a reduction in total breastfeeding of 1.4 (95% CI: 0.6; 2.1) months and perfluorooctanoic acid (PFOA) where a doubling was associated with a reduction in exclusive breastfeeding of 0.5 (0.3; 0.7) months. The associations were evident among both primiparous and multiparous women, and thus cannot be explained by confounding from previous breastfeeding.

Background The course of coronavirus disease 2019 (COVID-19) seems to be aggravated by air pollution, and some industrial chemicals, such as the perfluorinated alkylate substances (PFASs), are immunotoxic and may contribute to an association with disease severity. Methods From Danish biobanks, we obtained plasma samples from 323 subjects aged 30–70 years with known SARS-CoV-2 infection. The PFAS concentrations measured at the background exposures included five PFASs known to be immunotoxic. Register data was obtained to classify disease status, other health information, and demographic variables. We used ordered logistic regression analyses to determine associations between PFAS concentrations and disease outcome. Results Plasma-PFAS concentrations were higher in males, in subjects with Western European background, and tended to increase with age, but were not associated with the presence of chronic disease. Of the study population, 108 (33%) had not been hospitalized, and of those hospitalized, 53 (16%) had been in intensive care or were deceased. Among the five PFASs considered, perfluorobutanoic acid (PFBA) showed an unadjusted odds ratio (OR) of 2.19 (95% confidence interval, CI, 1.39–3.46) for increasing severities of the disease. Among those hospitalized, the fully adjusted OR for getting into intensive care or expiring was 5.18 (1.29, 20.72) when based on plasma samples obtained at the time of diagnosis or up to one week before. Conclusions Measures of individual exposures to immunotoxic PFASs included short-chain PFBA known to accumulate in the lungs. Elevated plasma-PFBA concentrations were associated with an increased risk of a more severe course of COVID-19. Given the low background exposure levels in this study, the role of exposure to PFASs in COVID-19 needs to be ascertained in populations with elevated exposures.

Background: The aim of this study was to determine whether measles, mumps and rubella (MMR) vaccination administered in early childhood was associated with asthma and allergic diseases at ages 5, 7 and 13 years in a birth cohort as the existing literature on the association between measles vaccination and allergic disease is inconclusive. Methods: In the Faroe Islands, 640 children were followed from birth. Follow-up examinations were performed at ages 5, 7 and 13 years. They included physical examinations and maternal questionnaires about the child’s health. At age 7 total and grass-specific IgE was quantified in serum, and at age 13 the children underwent skin prick tests (SPT). At the examinations the child’s vaccination card was reviewed. Results: At age 5, 533 of 555 children had been vaccinated for MMR. After confounder adjustment we found early life MMR vaccination to be associated with a two-third reduction in the odds of asthma (OR: 0.33, 95% CI: 0.12; 0.90) and hypersensitivity/allergy (OR: 0.32, 95% CI: 0.11; 0.88) at age 5, and the substantially decreased odds of asthma were replicated at age 13 (OR: 0.22, 95% CI: 0.08; 0.56). At age 7 serum total IgE was reduced by 62.8% (CI 95%: −84.3%; −11.9%) in the vaccinated children. MMR vaccination was not significantly associated with allergic rhinoconjuctivitis symptoms, eczema, or SPT reactions at age 13. Conclusions: MMR vaccination early in life may have a protective effect against allergy at least up to age 7 and against asthma through age 13 years.

Perfluoroalkyl substances (PFAS) are highly persistent chemicals that might be associated with asthma and allergy, but the associations remain unclear. Therefore, this study examined whether pre- and post-natal PFAS exposure was associated with childhood asthma and allergy. Measles, mumps and rubella (MMR) vaccination in early life may have a protective effect against asthma and allergy and is therefore taken into account when evaluating these associations. In a cohort of Faroese children whose mothers were recruited during pregnancy, serum concentrations of five PFAS were measured: Perfluorohexane sulfonic acid (PFHxS), perfluorooctane sulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), and perfluorodecanoic acid (PFDA) at three timepoints (maternal serum in pregnancy week 34–36 and child serum at ages 5 and 13 years) and determined their association with immunoglobulin E (IgE) (cord blood and at age 7 years) and asthma/allergic diseases (questionnaires at ages 5 and 13 years and skin prick test at age 13 years). A total of 559 children were included in the analyses. Interactions with MMR vaccination were evaluated. Among 22 MMR-unvaccinated children, higher levels of the five PFAS at age 5 years were associated with increased odds of asthma at ages 5 and 13. The associations were reversed among MMR-vaccinated children. Pre-natal PFAS exposure was not associated with childhood asthma or allergic diseases regardless of MMR vaccination status. In conclusion, PFAS exposure at age 5 was associated with increased risk of asthma among a small subgroup of MMR-unvaccinated children but not among MMR-vaccinated children. While PFAS exposure may impact immune system functions, this study suggests that MMR vaccination might be a potential effect-modifier.

Bacillus Calmette–Guérin (BCG) vaccine against tuberculosis (TB) is recommended at birth in TB‐endemic areas. Currently, BCG vaccination programmes use “BCG vaccination coverage by 12 months of age” as the performance indicator. Previous studies suggest that BCG‐vaccinated children, who develop a scar, have better overall survival compared with BCG‐vaccinated children, who do not develop a scar. We summarized the available studies of BCG scarring and child survival. A structured literature search for studies with original data and analysis of BCG scarring and mortality were performed. Combined analyses on the effect of BCG scarring on overall mortality. We identified six studies covering seven cohorts, all from Guinea‐Bissau, West Africa, with evaluation of BCG scarring amongst BCG‐vaccinated children and follow‐up for mortality. Determinants of BCG scarring were BCG strain, intradermal injection route, size of injection wheal, and co‐administered vaccines and micronutrients. In a combined analysis, having a BCG scar vs. no BCG scar was associated with a mortality rate ratio (MRR) of 0.61 (95% CI: 0.51–0.74). The proportion with a BCG scar varied from 52 to 93%; the estimated effect of a BCG scar was not associated with the scar prevalence. The effect was strongest in the first (MRR = 0.48 (0.37–0.62)) and second (MRR = 0.63 (0.44–0.92)) year of life, and in children BCG‐vaccinated in the neonatal period (MRR = 0.45 (0.36–0.55)). The effect was not explained by protection against TB. Confounding and genetic factors are unlikely to explain the strong association between BCG scarring and subsequent survival. Including “BCG scar prevalence” as a BCG vaccination programme performance indicator should be considered. The effect of revaccinating scar‐negative children should be studied.