In industrialized nations, human lead exposure has decreased significantly in recent decades. Nevertheless, due to its toxic effects, this heavy metal remains a public health concern with children and adolescents being particularly at risk. In Europe nowadays, oral intake via food and drinking water is the predominant exposure pathway for lead. The objective of the present study was to investigate the association between dietary factors and blood lead (PbB) level of 3- to 17-year-old children and adolescents living in Germany, using data from the fifth German Environmental Health Survey (GerES V) and the Child and Adolescent Health Survey (KiGGS Wave 2). GerES V and KiGGS Wave 2 are two national population-representative studies conducted between 2014 and 2017, including measurement of lead concentrations in blood from 720 children and adolescents aged 3–17 years (mean age = 10.21, SD age = 4.36). Using multiple linear regression, sociodemographic and environmental characteristics as well as dietary factors could be identified as significant exposure determinants of PbB concentrations. Lead intake via domestic tap water was the strongest predictor of elevated PbB levels with 27.6% (p-value< .001) higher concentrations of highest compared to none lead intake via tap water. Other foods which were found to be relevant to PbB levels were meat, fruit, and fruit juice. While meat or fruit consumption were each associated with about 13% (p-value < .05) lower PbB levels, fruit juice drinking was associated with up to 12.2% (p-value = .04) higher PbB levels. In conclusion, results indicate the importance of dietary habits for lead exposure in children and adolescents. To protect vulnerable groups, it is recommended that future research and lead-reducing measures pay more attention to dietary links.

While exposure to ambient particulate matter (PM) and nitrogen dioxide (NO₂) is thought to be associated with diseases via inflammatory response, the association between exposure to ozone, an oxidative pollutant, and inflammation has been less investigated.We analyzed associations between short-term exposure to ozone and three inflammatory biomarkers among children and adolescents.These cross-sectional analyses were based on two follow-ups of the GINIplus and LISA German birth cohorts. We included 1330 10-year-old and 1591 15-year-old participants. Fractional exhaled nitric oxide (FeNO) and high-sensitivity C-reactive protein (hs-CRP) were available for both age groups while interleukin (IL)-6 was measured at 10 years only. Maximum 8-h averages of ozone and daily average concentrations of NO₂ and PM with an aerodynamic diameter <10 μm (PM₁₀) were adopted from two background monitoring stations 0 (same day), 1, 2, 3, 5, 7, 10 and 14 days prior to the FeNO measurement or blood sampling. To assess associations, we utilized linear regression models for FeNO, and logistic regressions for IL-6 and hs-CRP, adjusting for potential covariates and co-pollutants NO₂ and PM₁₀.We found that short-term ozone exposure was robustly associated with higher FeNO in adolescents at age 15, but not at age 10. No consistent associations were observed between ozone and IL-6 in children aged 10 years. The relationship between hs-CRP levels and ozone was J-shaped. Relatively low ozone concentrations (e.g., <120 μg/m³) were associated with reduced hs-CRP levels, while high concentrations (e.g., ≥120 μg/m³) tended to be associated with elevated levels for both 10- and 15-year-old participants.Our study demonstrates significant associations between short-term ozone exposure and FeNO at 15 years of age and a J-shaped relationship between ozone and hs-CRP. The finding indicates that high ozone exposure may favor inflammatory responses in adolescents, especially regarding airway inflammation.

The effects of exposure to some environmental chemicals on blood pressure have been determined, but the association between non-occupational exposure to perfluoroalkyl substances (PFASs) and blood pressure in adolescents remains unknown. The association between blood pressure and PFAS concentrations was studied by analysing data from 2251 participants filtered from the population enrolled in the National Health and Nutrition Examination Survey (NHANES) from 2003 to 2012. After adjusting for age, sex, race, BMI, cotinine level, dietary intake of calcium, caloric intake, sodium consumption, potassium consumption and sampling year, we estimated the coefficients (betas) and 95% confidence intervals (CIs) for the relationship between PFAS concentrations and blood pressure with multiple linear regression models. Potential non-linear relationships were assessed with restricted cubic spline models. Blood levels of perfluorooctane sulfonic acid (PFOS) had a strong positive association with diastolic blood pressure (DBP) in adolescents in the linear model, while the result was not significant in the non-linear model. No significant association was observed between the concentration of any other PFASs and blood pressure. According to the fully adjusted linear regression model (P = 0.041), the mean DBP values in boys in the higher PFOS quintile were 2.70% greater than the mean DBP values of boys in the lowest PFOS quintile. Furthermore, serum PFOS concentrations predominantly affected blood pressure in male adolescents compared with female adolescents. These results provide epidemiological evidence of PFOS-related increases in DBP. Further research is needed to address related issues.

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.

Acrylonitrile is a colorless volatile liquid mostly present in tobacco smoke. Acrylonitrile exposure has shown to increase oxidative stress in animal studies; however, there was no previous research in human epidemiology. In this study, 853 subjects were recruited from a cohort of Taiwanese adolescents and young adults to investigate the association between urinary concentrations of the acrylonitrile metabolite N-acetyl-S-(2-cyanoethyl)-L-cysteine (CEMA), the oxidative stress product 8-hydroxydeoxyguanosine (8-OHdG) and cardiovascular disease (CVD) risk factors. The geometric mean (SD) of CEMA and 8-OHdG concentrations were 4.67 (8.61) μg/L and 2.97 (2.14) μg/L, respectively. 10% elevated in CEMA (μg/L) was positively correlated with the change of 8-OHdG levels (μg/L) (β = 0.325, SE = 0.105, P = 0.002) in multiple linear regression analyses. The urinary CEMA was not related to other CVD risk factors. In subpopulation analyses, the association between CEMA and 8-OHdG was evident in all genders, adolescents, homeostasis model assessment of insulin resistance score ≥0.89, and environmental tobacco smokers. In this study, we observed that higher levels of CEMA levels were correlated with increased levels of 8-OHdG in this cohort. Future research on exposure to acrylonitrile and oxidative stress was warranted.

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.

Although an association between urinary phthalate (PAE) metabolites and respiratory symptoms and diseases has been reported, knowledge regarding its effect on pulmonary function is limited, especially in adolescents. Using cross-sectional data from 1389 adolescents (aged 10–19 years) in the 2007–2012 National Health and Nutrition Examination Survey, the association of mixed urinary PAE metabolites with pulmonary function was evaluated using the weighted quantile sum. Moreover, multivariate linear regression was performed to investigate associations between each urinary PAE metabolite and pulmonary function indicators and to estimate the interaction effects between urinary PAE metabolites and demographic characteristics. We found that mixed urinary PAE metabolites were negatively associated with forced expiratory volume at the 1 s (FEV1, p < 0.001) and forced vital capacity (FVC, p = 0.008) levels. In individual PAE metabolite analyses, mono (carboxynonyl) pthalate (MCNP), mono-n-butyl pthalate (MnBP), mono-isobutyl pthalate (MiBP), mono-(2-ethyl-5-oxohexyl) phthalate (MEOHP) and mono-benzyl phthalate (MBzP) correlated negatively with both FVC and FEV1 values (Holm-Bonferroni corrected p < 0.05). Mono-(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) was negatively associated with the FVC value. Significant interactions between sex and urinary MnBP or MBzP levels for the risk of FEV1 decrease in girls were found (p = 0.005), as was a significant interaction between sex and urinary MBzP level for the risk of FVC decline. Our findings suggest that higher PAE exposure is associated with respiratory dysfunction; the association is more pronounced among girls.

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).

Few studies have explored the links of air pollution and childhood lipid profiles and dyslipidemias. We aimed to explore this topic in Chinese children and adolescents. This study included 12,814 children aged 7–18 years who participated in a national survey in 2013. Satellite-based spatial-temporal model was used to predict 3-y (2011–2013) average particles with diameters ≤ 1.0 μm (PM₁), ≤2.5 μm (PM₂.₅), ≤10 μm (PM₁₀), and nitrogen dioxide (NO₂) concentrations. Generalized linear mixed models were employed to evaluate the relationships of air pollution and total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and dyslipidemias. Every 10 μg/m³ increase in PM₁, PM₂.₅, PM₁₀, and NO₂ was related to increases of 6.20% [95% confidence interval (CI): 2.44, 10.10], 5.31% (95%CI: 0.41, 10.44), 3.49% (95%CI: 0.97, 6.08), and 5.25% (95%CI: 1.56, 9.07) in TC, respectively. The odds ratio of hypercholesterolemia associated with a 10 μg/m³ increase in PM₁, PM₂.₅, and NO₂ was 2.15 (95%CI: 1.27, 3.65), 1.70 (95%CI: 1.12, 2.60), and 1.43 (95%CI: 1.05, 1.93), respectively. No associations were found for air pollution and other blood lipids. Long-term PM₁, PM₂.₅, PM₁₀, and NO₂ exposures were positively associated with TC levels and risk of hypercholesterolemia in children and adolescents.

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.