Currently, studies on the association between per-/polyfluoroalkyl substances (PFAS) concentrations and the renal function of residents, especially teenagers, living near fluorochemical industrial plants, are relatively rare, and not all these studies suggested associations. In this cross-sectional study, 775 local teenagers (11–15 years old) were included, and serum concentrations of 18 PFAS were measured. Perfluorooctanoic acid (PFOA) was found to be the dominant PFAS with a concentration of 22.3–3310 ng/mL (mean = 191 ng/mL), accounting for 71.5–99.1% of ΣPFAS. Statistical analyses demonstrated that internal exposure of perfluoroalkyl carboxylic acids (PFCA, C8–C10) was related to the plant. In addition, the prevalence rate of chronic kidney disease (CKD) (35.0%) in the participants was relatively high. A significantly positive association was observed between the increase in PFOA concentration and increasing risk of CKD (OR = 1.741; 95% CI: 1.004, 3.088; p = 0.048) by adjusting for gender, age, body mass index (BMI), and household income. Similar positive correlation was also observed in PFHpA with CKD (OR = 1.628, 95% CI: 1.031, 2.572; p = 0.037). However, no significant correlation was observed for concentrations of other PFAS and CKD (p > 0.05). Furthermore, linear regression analyses demonstrated that none of the PFAS concentrations were significantly correlated with estimated glomerular filtration rate (eGFR) or urine albumin/urine creatinine ratio (ACR) (p > 0.05). However, a significantly negative correlation was observed between PFOA concentration and abnormal ACR (β = −0.141, 95% CI: −0.283, 0.001; p = 0.048) after stratifying by CKD. Sensitivity analyses further confirmed these results. This cross-sectional study is the first, to our knowledge, to investigate the association between PFAS concentrations and renal function in teenagers living near a Chinese industrial plant. Further prospective and metabonomic studies are needed to interpret the results and clarify the biological mechanisms underlying this association.

The association of co-exposure to polycyclic aromatic hydrocarbons (PAHs) and phthalates (PAEs) with blood cell-based inflammatory biomarkers is largely unknown. We conducted a panel study of 144 children aged 4–12 years, with up to 3 repeated visits across 3 seasons. For each visit, we collected the first-morning urine for 4 consecutive days and fasting blood on the day of physical examination. We developed a gas chromatography/tandem mass spectrometry method to detect the metabolites of 10 PAHs (OH-PAHs) and 10 PAEs (mPAEs) in urine samples. We employed linear mixed-effects models to evaluate the individual associations of each OH-PAH and mPAE with blood cell-based inflammatory biomarkers over different lag times. Bayesian kernel machine regression (BKMR) and quantile g-computation were used to evaluate the overall associations of OH-PAHs and mPAEs mixtures with blood cell-based inflammatory biomarkers. After multiple adjustments, we found positive associations of summed hydroxylphenanthrene (∑OHPHE), summed OH-PAHs, and mono-n-butyl phthalate with inflammatory biomarkers such as neutrophil count, neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, and the systemic immune-inflammation index (SII) at lag 0 (the day of physical examination). Each 1% increase in ∑OHPHE was related to a 0.18% (95% confidence interval: 0.10%, 0.25%) increase in SII, which was the strongest among the above associations. The results of BKMR and quantile g-computation suggested that co-exposure to PAHs and PAEs mixture was associated with an elevated white blood cell count, neutrophil count, neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, and SII, to which ∑OHPHE and 1-hydroxypyrene (1-OHPYR) might be the major contributors. In addition, gender and age modified the associations of ∑OHPHE and 1-OHPYR with inflammatory biomarkers, where girls and younger children were more susceptible. In conclusion, co-exposure to PAHs and PAEs was associated with elevated inflammation in children, in which ∑OHPHE and 1-OHPYR might play important roles.

Although short-term exposure to air pollution can trigger sudden heart attacks, evidence is scarce regarding the relationship between sub-daily changes in air pollution level and the risk of acute myocardial infarction (AMI). Here we assessed the intraday effect of air pollution on AMI risk and potential effect modification by pre-existing cardiac risk factors. Hourly data on emergency department visits (EDVs) for AMI and air pollutants in Brisbane, Australia during 2013–2015 were acquired from pertinent government departments. A time-stratified case-crossover analysis was adopted to examine relationships of AMI risk with hourly changes in particulate matters (aerodynamic diameter ≤ 2.5 μm (PM₂.₅) and ≤10 μm (PM₁₀)) and gaseous pollutants (ozone and nitrogen dioxide) after adjusting for potential confounders. We also conducted stratified analyses according to age, gender, disease history, season, and day/night time exposure. Excess risk of AMI per 10 μg/m³ increase in air pollutant concentration was reported at four time windows: within 1, 2–6, 7–12, and 13–24 h. Both single- and multi-pollutant models found an elevated risk of AMI within 2–6 h after exposure to PM₂.₅ (excessive risk: 12.34%, 95% confidence interval (CI): 1.44%–24.42% in single-pollutant model) and PM₁₀ within 1 h (excessive risk: 5.21%, 95% CI: 0.26%–10.40% in single-pollutant model). We did not find modification effect by age, gender, season or day/night time, except that PM₂.₅ had a greater effect on EDVs for AMI during night-time than daytime. Our findings suggest that AMI risk could increase within hours after exposure to particulate matters.

Investigating environmental pollution is important to understand its impact on endangered species such as green turtles (Chelonia mydas). In this study, we investigated the accumulation and potential toxicity of selected persistent organic pollutants (POPs) and naturally occurring MeO-PBDEs in liver, fat, kidney and muscle of turtles (n = 30) of different gender, size, year of death, location and health status. Overall, POP concentrations were low and accumulation was highest in liver and lowest in fat which is likely due to the poor health of several animals, causing a remobilization of lipids and associated compounds. PCBs and p,p’-DDE dominated the POP profiles, and relatively high MeO-PBDE concentrations (2′-MeO-BDE 68 up to 192 ng/g lw, 6-MeO-BDE 47 up to 79 ng/g lw) were detected in all tissues. Only few influences of factors such as age, gender and location were found. While concentrations were low compared to other marine wildlife, biological toxicity equivalences obtained by screening the tissue extracts using the micro-EROD assay ranged from 2.8 to 356 pg/g and the highest values were observed in muscle, followed by kidney and liver. This emphazises that pollutant mixtures found in the turtles have the potential to cause dioxin-like effects in these animals and that dioxin-like compounds should not be overlooked in future studies.

Phthalates (PAEs) are popular synthetic chemicals used as plasticizers and solvents for various products, such as polyvinyl chloride or personal care products. Human exposure to PAEs is associated with various diseases, resulting in PAE biomonitoring in humans. Inhalation, dietary ingestion, and dermal absorption are the major human exposure routes. However, estimating the actual exposure dose of PAEs via an external route is difficult. As a result, estimation by internal exposure has become the popular analytical methods to determine the concentrations of phthalate metabolites (mPAEs) in human matrices (such as urine, serum, breast milk, hair, and nails). The various exposure sources and patterns result in different composition profiles of PAEs in biomatrices, which vary from country to country. Nevertheless, the mPAEs of diethyl phthalate (DEP), di-n-butyl phthalate (DnBP), di-iso-butyl phthalate (DiBP), and di-(2-ethylhexyl) phthalate (DEHP) are predominant in the urine. These mPAEs have greater potential health risks for humans. Children have been observed to exhibit higher exposure risks to several mPAEs than adults. Besides age, other influencing factors for phthalate exposure are gender, jobs, and residential areas. Although many studies have reported biological monitoring of PAEs, only a few reviews that adequately summarized the reports are available. The current review appraised available studies on mPAE quantitation in human biomatrices and estimated the dose and health risks of phthalate exposure. While some countries lack biomonitoring data, some countries’ data do not reflect the current PAE exposure. Thence, future studies should involve frequent PAE biomonitoring to accurately estimate human exposure to PAEs, which will contribute to health risk assessments of human exposure to PAEs. Such would aid the formulation of corresponding regulations and restrictions by the government.

Pyrethroids are an important class of insecticides, and thousands of tons of these compounds are used in the United States every year. This study characterized exposures to pyrethroids and assessed demographic, socioeconomic, and lifestyle factors that modulate pyrethroid exposure using data from the National Health and Nutrition Examination Survey (NHANES) 2007–2012, a nationally representative survey of the non-institutionalized population of the United States. Urinary levels of commonly used biomarkers of pyrethroid exposure, including 3-phenoxybenzoic acid (3-PBA), 4-fluoro-3-phenoxybenzoic acid (F-PBA), and cis-dibromovinyl-dimethylcyclopropane carboxylic acid (DBCA), were determined by liquid chromatography-tandem mass spectrometry. The detection rate of 3-PBA, a nonspecific metabolite of several pyrethroids, was 78.1% in adults (N = 5233) and 79.3% in children (N = 2295). The detection rates of all other pyrethroid metabolites were <10%. The median urinary level of 3-PBA in adults was 0.47 μg/L (interquartile range, 0.14–1.22 μg/L). For children, the median urinary level was 0.49 μg/L (interquartile range, 0.17–1.29 μg/L). Age, gender, family income-to-poverty ratio (PIR), levels of physical activity, alcohol intake, and body mass index were associated with 3-PBA levels in adults. In children, age, gender, race/ethnicity, and PIR were associated with 3-PBA levels. 3-PBA levels also differed significantly across NHANES cycles, with higher levels observed in NHANES 2011–2012. Geometric mean 3-PBA levels in U.S. adults were 0.41 μg/L in NHANES 2007–2008, 0.41 μg/L in NHANES 2009–2010, and 0.66 μg/L in NHANES 2011–2012. In U.S. children, geometric mean 3-PBA levels were 0.40 μg/L in NHANES 2007–2008, 0.46 μg/L in NHANES 2009–2010, and 0.70 μg/L in NHANES 2011–2012. These results demonstrate that pyrethroid exposures remain a current environmental health concern and lay the foundation for further preclinical and epidemiological studies assessing human health risks associated with pyrethroids.

The aim of this study was to investigate environmental and lifestyle factors affecting exposure to PAHs in the general population in a large city of the Middle East (Tehran) by measuring urinary monohydroxy polycyclic aromatic hydrocarbons (OH-PAHs) and establishing relationships between PAHs exposure and related factors. Urine samples were collected from 222 randomly chosen subjects who were living in the urban area of Tehran, Iran. Subjects were required to complete a detailed questionnaire aimed to document their personal and sociodemographic information, activities, cooking-related appliances, smoking history/exposure, and consumed foodstuff. Identification and quantification of six OH-PAHs was carried out using a gas chromatography with mass spectrometry (GC-MS). The geometric means for 1-OHP, 1-NAP, 2-NAP, 2-FLU, 9-FLU, and 9-PHE for whole population study were 310, 1220, 3070, 530, 330, and 130 ng/g creatinine, respectively. The two naphthalene metabolites contributed on average 77% of the total concentration of six measured OH-PAHs, followed by the 2-FLU, 1-OHP, 9-FLU, and 9-PHE. The most important predictors of urinary PAHs were consumption of grilled/barbecued foods, smoking, and exposure to environmental tobacco smoking. Water pipe smoking was linked to urinary OH-PAH metabolite in a dose-response function. Residential traffic was also related with OH-PAH metabolite concentrations. Other factors including gender, age, exposure to common house insecticides, open burning, and candle burning were found to be statistically associated with the urinary levels of some OH-PAHs. High exposure to PAHs among general population in Middle Eastern large cities and its associated health implications calls for public health measures to reduce PAHs exposure.

Bisphenol A (BPA) is an endocrine-disrupting chemical. Studies have shown that the exposure to BPA is associated with attention-deficit/hyperactivity disorder (ADHD) during adolescent development. However the direct clinical evidence is limited. To investigate the possible association between environmental BPA exposure and the altered behavior of children, a case-control study was conducted with children aged 6–12 years in Guangzhou, China. Two hundred fifteen children diagnosed with ADHD and 253 healthy children from Guangzhou were recruited as the case and control groups, respectively. Urinary BPA and 8-hydroxy-2′-deoxyguanosine (8-OHdG, a biomarker of oxidative DNA damage) concentrations were determined by high-performance liquid chromatography/tandem spectrometry. The results showed that concentrations of urinary BPA for the case group were significantly higher than those for the control group (3.44 vs 1.70 μg/L; 4.63 vs 1.71 μg/g Crt. p < .001). A stepwise increase in the odds ratios for ADHD was observed with the increasing quartiles of children's urinary BPA (first quartile: reference category; second quartile adjusted OR: 1.79, 95% CI: 0.95–3.37; third quartile adjusted OR: 7.44, 95% CI: 3.91–14.1; fourth quartile adjusted OR: 9.41, 95% CI: 4.91–18.1). When the BPA levels were stratified by gender, the odds of ADHD among boys and girls increased significantly with urinary BPA concentrations (adjusted OR: 4.58, 95% CI: 2.84–7.37; adjusted OR: 2.83, 95% CI: 1.17–6.84). Urinary 8-OHdG concentrations in the ADHD children were significantly higher than those in the control group. Furthermore, the linear regression analysis results indicated that a significant relationship existed between BPA exposure and 8-OHdG levels (R = 0.257, p < .001). Our findings provide direct evidence that childhood BPA exposure may be related to ADHD and 8-OHdG concentrations for children. Moreover, BPA exposure could increase the higher occurrence of ADHD for boy than for girls.

Acrylamide-induced immunotoxicity and allergic dermatitis have been reported in animal experiments and clinical reports, respectively. However, epidemiological evidence from the general population is limited.The purpose of the present study was to estimate the associations between acrylamide exposure and allergy-related outcomes in the general US population.A total of 6982 subjects were selected from the National Health and Nutrition Examination Survey 2005–2006 (NHANES). Internal exposure was measured by the hemoglobin adducts of acrylamide (HbAA) and its metabolite glycidamide (HbGA). Allergy-related outcomes including asthma, hay fever, allergy, itchy rash, sneeze, wheeze and eczema were obtained by self-administered questionnaires. Allergic sensitization was assessed by the total immunoglobulin E (IgE) levels. The associations of HbAA and HbGA quartiles with allergy-related outcomes were calculated using logistic regression models with multivariable adjustments. Analyses were additionally stratified according to age, gender and serum cotinine levels.When setting quartile 1 of HbAA as reference, the odds ratios (ORs) [95% confidence intervals (CIs)] of quartile 2 to 4 for eczema were 1.18 (0.79–1.76), 1.14 (0.73–1.78) and 1.58 (1.14–2.18), respectively (ptrend = 0.002). Individuals at the highest quartile of HbGA had significantly elevated likelihoods of itchy rash (OR = 1.37, 95% CI = 1.02–1.83, ptrend = 0.032) and eczema (OR = 1.45, 95% CI = 1.06–1.97, ptrend = 0.044). The stratification analyses indicated various results in different subgroups.This study indicated significant associations between HbAA and HbGA levels and the likelihoods of allergy-related outcomes in the general US population, depending on age, gender and smoke exposure status. These findings suggested potential public health concerns for the widespread exposure to acrylamide.

To investigate the risk of hyperuricemia in relation to Perfluoroalkyl substances (PFASs) in children from Taiwan, 225 Taiwanese children aged 12–15 years were recruited from 2009 to 2010. Linear and logistic regression models were employed to examine the influence of PFASs on serum uric acid levels. Findings revealed that eight of ten PFASs analyses were detected in >94% of the participants' serum samples. Multivariate linear regression models revealed that perfluorooctanic acid (PFOA) was positively associated with serum uric acid levels (β = 0.1463, p < 0.05). Of all the PFASs analyses, only PFOA showed a significant effect on elevated levels of hyperuricemia (aOR = 2.16, 95%CI: 1.29–3.61). When stratified by gender, the association between serum PFOA and uric acid levels was only evident among boys (aOR = 2.76, 95%CI: 1.37–5.56). In conclusion, PFOA was found to be associated with elevated serum levels of uric acid in Taiwanese children, especially boys. Further research is needed to elucidate these links.