Persistent and mobile chemicals (PMs) and per- and polyfluoroalkyl substances (PFAS) are groups of chemicals that have received recent global attention due to their potential health effects on the environment and humans. In this study, exposure to a broad range of PMs and PFAS was investigated in Flemish adolescents’ urine samples (n = 83) using a suspect screening approach. For this purpose, three sample preparation methods were evaluated, and a basic liquid-liquid extraction was optimized for urine analysis based on the extraction efficiency of PMs (53–80%) and PFAS (>70%). In total, 9 PMs were identified in urine samples at confidence levels (CL) 1–3 and, among them, acetaminophen, 4-aminophenol, 2,2,6,6-tetramethyl-4-piperidone, trifluoroacetic acid (TFAA), sulisobenzone, ethyl sulfate, and 1,2-benzisothiazol-3(2H)-one 1,1-dioxide were confirmed at CL 1 and 2. In addition, the detection and identification of 2,2,6,6-tetramethyl-4-piperidone, 4-aminophenol, TFAA, and m-(2,3-epoxypropoxy)-N,N-bis(2,3-epoxypropyl) aniline (CL 3), has been reported for the first time in human urine in this study. For PFAS, only 2 compounds were identified at CL 4, implying that urine is not a suitable matrix for suspect screening of such compounds. A significant difference between sexes was observed in the detection rate of identified PMs, in particular for acetaminophen, 4-aminophenol, and sulisobenzone. The findings of this study can be used in future human biomonitoring programs, such as by including the newly identified compounds in quantitative methods or monitoring in other human matrices (e.g., serum).

An increasing number of epidemiological studies have examined air pollution as a possible contributor to adverse sleep health, but results are mixed. The aims of this systematic review are to investigate and summarize the associations between exposures to air pollutants and various sleep measures across the lifespan. PubMed, CINAHL, Cochrane, Scopus, Web of Science, and PsycInfo were searched through October 2019 to identify original data-based research examining direct epidemiological associations between ambient and indoor air pollution exposures and various sleep health measures, including sleep quality, sleep duration, sleep disturbances, and daytime sleepiness. Twenty-two articles from 2010 to 2019 were selected for inclusion in this review, including a wide range of study populations (from early childhood to elderly) and locations (10 Asian, 4 North American, 3 European, 5 other). Due to variation in both exposure and outcome assessments, conducting a meta-analysis was not plausible. Twenty-one studies reported a generally positive association between exposure and poor sleep quality. While most studies focused on ambient air pollutants, five assessed the specific effect of indoor exposure. In children and adolescents, increased exposure to both ambient and indoor pollutants is associated with increased respiratory sleep problems and a variety of additional adverse sleep outcomes. In adults, air pollution exposure was most notably related to sleep disordered breathing. Existing literature generally shows a negative relationship between exposures to air pollution and sleep health in populations across different age groups, countries, and measures. While many associations between air pollution and sleep outcomes have been investigated, the mixed study methods and use of subjective air pollution and sleep measures result in a wide range of specific associations. Plausible toxicological mechanisms remain inconclusive. Future studies utilizing objective sleep measures and controlling for all air pollution exposures and individual encounters may help ameliorate variability in the results reported by current published literature.

Little information exists on interaction effects between air pollution and influenza vaccination on allergic respiratory diseases. We conducted a large population-based study to evaluate the interaction effects between influenza vaccination and long-term exposure to ambient air pollution on allergic respiratory diseases in children and adolescents.A cross-sectional study was investigated during 2012–2013 in 94 schools from Seven Northeastern Cities (SNEC) in China. Questionnaires surveys were obtained from 56 137 children and adolescents aged 2–17 years. Influenza vaccination was defined as receipt of the influenza vaccine. We estimated air pollutants exposure [nitrogen dioxide (NO2) and particulate matter with aerodynamic diameters ≤1 μm (PM1), ≤2.5 μm (PM2.5) and ≤10 μm (PM10)] using machine learning methods. We employed two-level generalized linear mix effects model to examine interactive effects between influenza vaccination and air pollution exposure on allergic respiratory diseases (asthma, asthma-related symptoms and allergic rhinitis), after controlling for important covariates.We found statistically significant interactions between influenza vaccination and air pollutants on allergic respiratory diseases and related symptoms (doctor-diagnosed asthma, current wheeze, wheeze, persistent phlegm and allergic rhinitis). The adjusted ORs for doctor-diagnosed asthma, current wheeze and allergic rhinitis among the unvaccinated group per interquartile range (IQR) increase in PM1 and PM2.5 were significantly higher than the corresponding ORs among the vaccinated group [For PM1, doctor-diagnosed asthma: OR: 1.89 (95%CI: 1.57–2.27) vs 1.65 (95%CI: 1.36–2.00); current wheeze: OR: 1.50 (95%CI: 1.22–1.85) vs 1.10 (95%CI: 0.89–1.37); allergic rhinitis: OR: 1.38 (95%CI: 1.15–1.66) vs 1.21 (95%CI: 1.00–1.46). For PM2.5, doctor-diagnosed asthma: OR: 1.81 (95%CI: 1.52–2.14) vs 1.57 (95%CI: 1.32–1.88); current wheeze: OR: 1.46 (95%CI: 1.21–1.76) vs 1.11 (95%CI: 0.91–1.35); allergic rhinitis: OR: 1.35 (95%CI: 1.14–1.60) vs 1.19 (95%CI: 1.00–1.42)]. The similar patterns were observed for wheeze and persistent phlegm. The corresponding p values for interactions were less than 0.05, respectively. We assessed the risks of PM1-related and PM2.5-related current wheeze were decreased by 26.67% (95%CI: 1.04%–45.66%) and 23.97% (95%CI: 0.21%–42.08%) respectively, which was attributable to influenza vaccination (both p for efficiency <0.05).Influenza vaccination may play an important role in mitigating the detrimental effects of long-term exposure to ambient air pollution on childhood allergic respiratory diseases. Policy targeted at increasing influenza vaccination may yield co-benefits in terms of reduced allergic respiratory diseases.

The link between phthalate exposure and the risk of subclinical atherosclerosis in young population remains unclear. This study investigated the association between phthalate exposure and subclinical atherosclerosis, in terms of carotid intima-media thickness (CIMT), in young population. From a nationwide mass urine screening for renal health, conducted in 1992–2000 among school children 6–18 years of age in Taiwan, we recruited 789 subjects to participate in the cardiovascular health examination in 2006–2008. Among them, 787 received measurements of 7 urinary phthalate metabolites and CIMT. Results showed both mean and maximal values of CIMT at all segments of carotid arteries significantly increased with the urinary mono-2-ethylhexyl phthalate (MEHP), ∑ di-(2-ethylhexyl) phthalate (DEHP), and mono-n-butyl phthalate (MnBP) in a dose-response relationship after adjustment for multiple linear regression models. Multivariate logistic regression analysis showed that higher quartiles of urinary concentrations of MEHP, ∑DEHP, and MnBP were associated with a higher risk of thicker CIMT. Compared to subjects with the lowest quartile (Q1) of urinary MEHP, the adjusted odds ratios (95% confidence interval) for thicker CIMT among subjects with higher urinary MEHP were 2.13 (1.18–3.84) at Q2, 4.02 (2.26–7.15) at Q3 and 7.39 (4.16–13.12) at the highest Q4. In conclusion, urinary phthalate metabolites of MEHP, ∑DEHP, and MnBP are strongly associated with CIMT in adolescents and young adults in Taiwan.

Inhalation exposure to flame retardants used as additives to minimize fire risk and plasticizers is ubiquitous in human daily activities, but has not been adequately assessed. To address this research gap, the present study conducted an assessment of human health risk for four age groups through inhalation exposure to size fractionated particle-bound and gaseous halogenated flame retardants (polybrominated diphenyl ethers (PBDEs) and alternative halogenated flame retardants (AHFRs)) and organophosphate esters (OPEs) at indoor and outdoor environments (school, office, and residence) in three districts of a megacity (Guangzhou, China). Results demonstrated that OPEs were the dominant components among all targets. Indoor daily intakes of PBDEs and OPEs were 13–16 times greater than outdoor levels for all age groups. Gaseous OPEs contributed significantly greater than particle-bound compounds to daily intakes of all target compounds. Based on the different life scenarios, hazard quotient (HQ) and incremental life cancer risk (ILCR) from adults exposure to PBDEs and OPEs in indoor and outdoor settings were the greatest, followed by adolescents, children, and seniors. The estimated HQ and ILCR for all age groups both indoors and outdoors were lower than the safe level (HQ = 1 and ILCR = 10−6), indicating that the potential health risk for local residents in Guangzhou via inhalation exposure to atmospheric halogenated flame retardants and OPEs was low.

Per- and polyfluoroalkyl Substances (PFAS) are ubiquitous in the environmental matrix, and their eco-toxicity on wide life and health risks on humans arising concerns. Due to the information gap, current risk assessments of PFAS ignore the indoor exposure pathway such as indoor dust and the different sources of drinking water. We collected and analyzed 168 indoor dust and 27 drinking water samples (including tap water, filtered water and bottled water). The mean concentrations of six typical PFAS measured in indoor dust and drinking water are in the range of 15.13–491.07 ng g⁻¹ and 0.31–4.14 ng L⁻¹, respectively. For drinking water, PFOA and PFOS were the dominant compounds, while PFHxS was the most abundant in indoor dust. Short-chain PFAS concentrations were higher than long-chain PFAS in both drinking water and indoor dust. Higher concentration of PFAS was observed in tap water and filtered water than bottled water. The total daily intake (TDI) of six PFAS are 20.67–52.97 ng kg⁻¹ d⁻¹ for infants, children, teenagers, and adults. As to children, teenagers, and adults, perfluorooctanoate (PFOA) is the major compound, accounting for 72.9–74.7% of the total daily intake. And PFOA (38.7%) and perfluorooctane sulfonate (PFOS, 42.2%) are the dominant PFAS for infants. The quantitative proportions of exposure sources are firstly revealed in this study, which in the order of foodstuff > indoor dust > drinking water > indoor air. Although the contribution to the PFAS intake of drinking water and indoor dust was not predominant (<9%), the health risks caused by long-term exposure need our attention. The hazard quotient (HQ) values of total PFAS were in the range of 0.154–0.498, which suggesting the relatively lower exposure risk in Chinese population. This study provides important reference to understand PFAS exposure status other than foodstuff.

Perfluoroalkyl acids (PFAAs) are persistent in the environment, highly bio-accumulative in the body, and likely hepatotoxic in humans. There is evidence of sex-specific physiological responses to PFAA exposure. However, epidemiological studies seldom stratify the analyses by sex. Given the high prevalence of liver disease in general population adolescents, this study was designed to determine whether or not there is association between exposure to PFAAs and biomarkers of liver function in adolescent participants of the 2013–2016 National Health and Nutrition Examination Survey, and whether or not such association is sex-specific. Multivariate linear regressions were performed to examine the association between single PFAAs [perfluorooctane sulfonic acid (PFOS); linear form of perfluorooctanoic acid (PFOA); perfluorohexane sulfonic acid (PFHxS); perfluorononanoic acid (PFNA)], and biomarkers of liver function — gamma glutamyltransferase (GGT), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total bilirubin. Multivariate logistic regressions were performed to estimate adjusted odd ratios (aOR) of elevated ALT, AST and GGT. The study results show that, in females, there was a positive association of the highest PFOA quartile with increased ALT, AST and GGT, and the highest PFNA quartile with increased ALT and AST. Conversely, in male adolescents there was an association of the highest linear PFOA quartile with decreased ALT, and the highest PFNA quartile with ALT and AST. Females had higher odds of clinically-defined elevated ALT with increased PFOA (aOR = 1.79; 95% CI: 1.05, 3.04) or PFNA (aOR = 2.28; 95% CI: 1.08, 2.28), whereas males had decreased odds of clinically-defined elevated ALT with increased n-PFOA (aOR = 0.43; 95% CI: 0.20, 0.93) or PFNA (aOR = 0.5; 95% CI: 0.28, 0.89). In conclusion, there were sex differences in the association between serum PFAA levels and biomarkers of liver function. These results may provide support for analyzing sex-based adverse effects of PFAAs.

Tin is a naturally occurring heavy metal that occurs in the environment in both inorganic and organic forms. Human exposure to tin is almost ubiquitous; however, surprisingly little is known about factors affecting environmental tin exposure in humans. This study analyzed demographic, socioeconomic and lifestyle factors associated with total urinary tin levels in adults (N = 3522) and children (N = 1641) participating in the National Health and Nutrition Examination Survey (NHANES) 2011–2014, a nationally representative health survey in the United States. Urinary tin levels, a commonly used biomarker of environmental tin exposure, were determined by inductively coupled plasma mass spectrometry (ICP-MS). Detection frequencies of tin were 87.05% in adults and 91.29% in children. Median and geometric mean levels of urinary tin in the adult population were 0.42 μg/L and 0.49 μg/L, respectively. For children, median and geometric mean levels of urinary tin were 0.60 μg/L and 0.66 μg/L, respectively. Age was identified as an important factor associated with urinary tin levels. Median tin levels in the ≥60 year age group were almost 2-fold higher than the 20–39 year age group. Tin levels in children were 2-fold higher than in adolescents. Race/ethnicity and household income were associated with tin levels in both adults and children. In addition, physical activity was inversely associated with urinary tin levels in adults. These results demonstrate that total tin exposures vary across different segments of the general U.S. population. Because the present study does not distinguish between organic and inorganic forms of tin, further studies are needed to better characterize modifiable factors associated with exposures to specific tin compounds, with the goal of reducing the overall exposure of the U.S. population.

Organophosphate esters (OPEs) are widely used in household products as flame retardants or plasticizers and have become ubiquitous pollutants in environmental media. However, little is known about OPE metabolites in humans, especially in children. In this study, eight OPE metabolites were measured in 411 urine samples collected from 6 to 14-year-old children in South China. Bis(2-chloroethyl) phosphate (BCEP), bis(1-chloro-2-propyl) phosphate (BCIPP) and diphenyl phosphate (DPHP) were the dominant OPE metabolites, and their median concentrations were 1.04, 0.15 and 0.28 μg/L, respectively. The levels of urinary OPE metabolites in the present study were much lower than those in participants from other countries, with the exception of BCEP, suggesting widespread exposure to tris(2-chlorethyl) phosphate (TCEP, the parent chemical of BCEP) in South China. No significant difference in the concentrations of any of the OPE metabolites was observed between males and females (p > .05). Significant negative correlations were observed between age and BCEP, BCIPP, bis(1,3-dichloro-2-propyl) phosphate (BDCIPP), di-o-cresyl phosphate (DoCP) and di-p-cresyl phosphate (DpCP) (DCP), or DPHP (p < .05). Pearson correlation coefficients between urinary OPE metabolites indicated multiple sources and OPE exposure pathways in children. The estimated daily intake suggested that children in South China have a relatively high exposure level to TCEP. To the best of our knowledge, this is the first study to report the urinary levels of OPE metabolites in Chinese children.

Dietary consumption of contaminated vegetables may contribute to polycyclic aromatic hydrocarbon (PAH) exposure in humans; however, this exposure pathway has not been examined thoroughly. This study aims to characterize the concentrations of PAHs in six types of vegetables grown near industrial facilities in Shanghai, China. We analyzed 16 individual PAHs on the US EPA priority list, and the total concentration in vegetables ranged from 65.7 to 458.0 ng g−1 in the following order: leafy vegetables (romaine lettuce, Chinese cabbage and Shanghai green cabbage) > stem vegetables (lettuce) > seed and pod vegetables (broad bean) > rhizome vegetables (daikon). Vegetable species, wind direction, and local anthropogenic emissions were determinants of PAH concentrations in the edible part of the vegetable. Using isomer ratios and principal component analysis, PAHs in the vegetables were determined to be mainly from coal and wood combustion. The sources of PAHs in the six types of vegetables varied. Daily ingestion of PAHs due to dietary consumption of these vegetables ranged from 0.71 to 14.06 ng d−1 kg−1, with contributions from Chinese cabbage > broad bean > romaine > Shanghai green cabbage > lettuce > daikon. The daily intake doses adjusted by body weight in children were higher than those in teenagers and adults. Moreover, in adults, higher concentrations of PAHs were found in females than in males. For individuals of different age and gender, the incremental lifetime cancer risks (ILCRs) from consuming these six vegetables ranged from 4.47 × 10−7 to 6.39 × 10−5. Most were higher than the acceptable risk level of 1 × 10−6. Our findings demonstrate that planting vegetables near industrial facilities may pose potential cancer risks to those who consume the vegetables.