Adults are mainly exposed to per- and polyfluoroalkyl substances (PFASs) via ingestion of food, inhalation of air and ingestion of dust, whereas for children the exposure to PFASs is largely unknown. This study aimed to reconstruct the serum concentrations of perfluorooctanoic acid (PFOA), perfluorooctane sulfonic acid (PFOS) and perfluorohexane sulfonic acid (PFHxS) in children after infancy up to 10.5 years of age and to test if dietary intake is the major exposure pathway for children to PFOA, PFOS and PFHxS after infancy. For this work, a dataset from a Finnish child cohort study was available, which comprised serum concentrations of the studied perfluoroalkyl acids (PFAAs) and PFAS concentration measurements in dust and air samples from the children's bedrooms. The calculated PFAA intakes were used in a pharmacokinetic model to reconstruct the PFAA serum concentrations from 1 to 10.5 years of age. The calculated PFOA and PFOS intakes were close to current regulatory intake thresholds and diet was the major exposure medium for the 10.5 year-olds. The one-compartment PK model reconstructed median PFOA and PFOS serum concentrations well compared to corresponding measured median serum concentrations, while the modelled PFHxS serum concentrations showed a constant underestimation. The results imply that children's exposure to PFOA and PFOS after breastfeeding and with increasing age resembles the exposure of adults. Further, the children in the Finnish cohort experienced a rather constant exposure to PFOA and PFOS between 1 and 10.5 years of age. The PFHxS exposure sources and respective pharmacokinetic parameter estimations need further investigation.

Per- and polyfluoroalkyl substances (PFASs) are highly stable, surface active chemicals, which are water- and oil/stain-repellent. Because of their unique properties, PFASs are widely used in consumer products. Their application ranges from personal-care products, food packaging and textiles to interior materials, thus leading to a continuous human exposure to PFASs in every-day life. Possible exposure pathways are the ingestion of food, drinking water and dust; the inhalation of fine dust and air; as well as dermal absorption after contact with the products and dust.

Despite the increasing number of monitoring studies, including measurement of concentrations in human exposure media and blood, childhood exposure is poorly understood.

The state of current knowledge on childhood exposure was investigated in paper I, by reviewing existing PFAS literature on exposure media, on daily intakes via different exposure pathways and on levels in blood and serum. Subsequently, recommendations for future research needs were made and implications presented on the regulation and assessment of PFASs. For paper II, III and IV, a cohort of background-exposed Finnish children was followed throughout childhood. Indoor air and floor dust samples of their bedrooms were taken at the age of 10.5 years in 2014/2015 and analysed for a wide range of PFASs (paper II and III). The estimated daily intakes (EDIs) via these two media were calculated in paper III. The EDIs revealed that dust ingestion and air inhalation are of similar importance for the intake of single perfluoroalkyl acids (PFAA), if the metabolism of PFAA precursors to PFAAs was included. The metabolism of precursors contributed considerably to the total intake of PFAAs via the inhalation of air (e.g. 38 % for perfluorooctanoic acid (PFOA) and 90 % for perfluorooctane sulfonic acid (PFOS)) and to the total intake of PFOS via the ingestion of dust (69 %; median values at the intermediate exposure scenario). In paper IV, the internal exposure during childhood was monitored by measuring serum concentrations, which were decreasing with age; and by calculating body burdens at 1, 6 and 10.5 years of age, which were constant or increasing, depending on the respective PFAS. These results demonstrated that it is crucial to account for growth dilution when studying exposure trends and PFAS intakes during childhood.

This thesis contributes to a better understanding of children’s exposure to PFASs, especially the internal exposure during childhood and the relative importance of both, indoor exposure pathways, as well as individual PFASs.

Studies suggest negative health impacts from early life exposure to per- and polyfluoroalkyl substances (PFASs). However, information on longitudinal exposure to PFASs during childhood is scarce for background-exposed individuals. This study sought to fill this gap by investigating children's longitudinal exposure trends through measurement of PFAS serum concentrations and calculation of body burdens (mu g, total in body). Blood of 54 Finnish children was sampled 2005-2015 and analyzed for 20 PFASs at 1, 6 and 10.5 years of age. The body burden was calculated by multiplying the serum concentration by the volume of distribution and the bodyweight for each individual. Associations between serum concentrations or body burdens and parameters, such as sex, breastfeeding duration, body mass index as well as indoor dust and air PFAS concentrations, were evaluated. Serum concentrations of perfluorooctane sulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA) and perfluorohexane sulfonic acid (PFHxS) decreased significantly (p < 0.001) with age. In contrast to serum concentrations, body burdens stayed unchanged or even increased significantly (p < 0.05), except for PFOA in female children. Breastfeeding duration was positively correlated (p < 0.001) with serum concentrations of PFHxS, PFOS, PFOA and PFNA at 1 year of age. Some associations were found at 10.5 years with sex and indoor PFAS concentrations. Observations of longitudinal decreasing trends of serum concentrations can be misleading for understanding exposure levels from external media during childhood, as the serum concentration is influenced by parallel temporal changes and growth dilution. Body burdens account for growth dilution and thus better reflect differences in early-life to adolescence exposure than serum concentrations.

We analysed floor dust samples from 65 children's bedrooms in Finland collected in 2014/2015 for 62 different per- and polyfluoroalkyl substances (PFASs) with a simple and highly efficient method. Validation results from the analysis of standard reference material (SRM) 2585 were in good agreement with literature data, while 24 PFASs were quantified for the first time. In the dust samples from children's bedrooms, five perfluoroalkyl carboxylic acids (PFCAs) and perfluorooctane sulfonic acid (PFOS) were detected in more than half of the samples with the highest median concentration of 5.26 ng/g for perfluorooctanoic acid (PFOA). However, the dust samples were dominated by polyfluoroalkyl phosphoric acid esters (PAPs) and fluorotelomer alcohols (FTOHs) (highest medians: 53.9 ng/g for 6:2 diPAP and 45.7 ng/g for 8:2 FTOH). Several significant and strong correlations (up to p = 0.95) were found among different PFASs in dust as well as between PFASs in dust and air samples (previously published) from the same rooms. The logarithm of dust to air concentrations (log K-dust/air) plotted against the logarithm of the octanol-air partition coefficient (log K-oa) resulted in a significant linear regression line with R-2 > 0.88. Higher dust levels of PFOS were detected in rooms with plastic flooring material in comparison to wood (p < 0.05). Total estimated daily intakes via dust (EDIdust) and air (EDIair) of perfluoroalkyl acids (PFAA), including biotransformation of precursors to PFAAs, were calculated for 10.5-year-old children. The total EDIdust, for PFOA and PFOS were estimated to be 0.007 ng/kg bw/day and 0.006 ng/kg bw/day, respectively, in an intermediate exposure scenario. The sum of the total EDIs for all PFAAs was slightly higher for dust than air (0.027 and 0.019 ng/kg bw/day). Precursor biotransformation was generally important for total PFOS intake, while for the PFCAs, FTOH biotransformation was estimated to be important for air, but not for dust exposure.

Due to the dynamic developmental processes during pregnancy, infancy, childhood and adolescence, exposure to PFASs is hypothesized to have the most pronounced negative effects during this period. In this review we critically evaluate the current state of the science regarding human early life exposure processes (until 18 years of age) to per- and polyfluoroalkyl substances (PFASs). Efficient placental transfer of perfluoroalkyl acids (PFAAs) results in relatively high prenatal exposure compared with many neutral organic contaminants. The few biomonitoring studies that specifically target infants, toddlers and other children suggest relatively high serum concentrations of perfluorooctane sulfonic acid (PFOS) and perfluorooctanoic acid (PFOA) in early life with peak concentrations occurring sometime before the child reaches 20 months. This peak in serum concentrations is most likely explained by exposure via breastfeeding, ingestion of house dust and/or specific contact events with consumer products leading to high body weight normalized estimated daily intakes (EDIs). Although children have higher EDIs of PFASs than adults, these are not always reflected by higher serum levels of PFASs in children in cross-sectional biomonitoring studies due to the confounding effect of age and birth cohort, and different exposure histories due to production changes. Longitudinal exposure studies measuring internal and external exposure (for multiple pathways and PFASs) at several time points during early life are strongly encouraged to understand temporal changes in exposure of individual children. A better quantitative understanding of early life exposure processes would help to improve the validity of epidemiological studies and allow informed decisions regarding setting of regulatory thresholds and appropriate mitigation actions.

The contamination levels and patterns of perfluoroallcyl acids (PFAAs) and their precursors in indoor air of children's bedrooms in Finland, Northern Europe, were investigated. Our study is among the most comprehensive indoor air monitoring studies (n = 57) and to our knowledge the first one to analyse air in children's bedrooms for PFASs (17 PFAAs and 9 precursors, including two acrylates, 6:2 FTAC and 6:2 FTMAC). The most frequently detected compound was 8:2 fluorotelomer alcohol (8:2 FTOH) with the highest median concentration (3570 pg/m(3)). FTOH concentrations were generally similar to previous studies, indicating that in 2014/2015 the impact of the industrial transition had been minor on FTOH levels in indoor air. However, in contrast to earlier studies (with one exception), median concentrations of 6:2 FTOH were higher than 10:2 FTOH. The C8 PFAAs are still the most abundant acids, even though they have now been phased out by major manufacturers. The mean concentrations of FOSE/As, especially MeFOSE (89.9 pg/m(3)), were at least an order of magnitude lower compared to previous studies. Collectively the comparison of FTOHs, PFAAs and FOSE/FOSAs with previous studies indicates that indoor air levels of PFASs display a time lag to changes in production of several years. This is the first indoor air study investigating 6:2 FTMAC, which was frequently detected (58%) and displayed some of the highest maximum concentrations (13 000 pg/m(3)). There were several statistically significant correlations between particular house and room characteristics and PFAS concentrations, most interestingly higher EtFOSE air concentrations in rooms with plastic floors compared to wood or laminate.