Infant exposure to per/polyfluoroalkyl compounds is associated with immune disruption. We examined associations between neonatal concentrations of perflurooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS) and immunoglobulin (Ig) isotype profiles in a prospective cohort of infants. We measured Ig isotypes, including IgA, IgE, IgM and the IgG subclasses IgG₁, IgG₂, IgG₃, and IgG₄, and PFOA and PFOS in newborn dried bloodspots from N = 3175 infants in the Upstate KIDS Study (2008–2010). We examined the association between newborn Ig isotype levels and individual PFOS and PFOA concentrations using mixed effects regression models with a random intercept to account for twins among study participants. We assessed the joint effect PFOA and PFOS with quantile-based g-computation on all singletons and one randomly selected twin (N = 2901), with Ig categorized as above or below median value. Models were adjusted for infant sex, and maternal pre-pregnancy body mass index, race, parity, age and infertility treatment. In adjusted models, PFOA was inversely associated with IgE (coefficient = −0.12 per unit increase in PFOA, 95% CI: −0.065, −0.17), whereas IgG₂, IgM, and IgA were positively associated with PFOA (coefficient for IgG₂ = 0.22, 95% CI: 0.15, 0.27; coefficient for IgM = 0.11, 95% CI: 0.08, 0.15; and coefficient for IgA = 0.15, 95% CI: 0.07, 0.18). There was no relation between PFOS and Ig isotypes. Analysis of the joint effect of PFOA and PFOS showed an OR of 1.2 (95% CI: 1.04, 1.36) for IgA and OR of 1.12 (95% CI: 1.00, 1.24) for IgG₂ levels above the median for every quartile increase. PFOA levels were significantly associated with elevated IgA, IgM, IgG₂, and reduced levels of IgE in single-pollutant models. A small but significant joint effect of PFOA and PFOS was observed. Our results suggest that early exposure to PFOA and PFOS may disrupt neonatal immunoglobulin levels.

Polycyclic aromatic hydrocarbons (PAHs) and certain ingredients in personal care products, such as parabens, bisphenols, triclosan and phthalate metabolites, have become ubiquitous in the world. Concerns of human exposure to these pollutants have increased during recent years because of various adverse health effects of these chemicals. Multiple compounds including parabens, bisphenols, triclosan, phthalate metabolites (mPAEs) and hydroxyl PAHs (OH-PAHs) in urine samples from Guangzhou were determined simultaneously to identify the human exposure pathways without external exposure data combined with data analysis, and the toxicants posed the highest risk to human health were screened in the present study. The detection frequencies for the chemicals exceeded 90%. Among the contaminants, mPAEs showed the highest concentrations, followed by OH-PAHs, with triclosan present at the lowest concentrations. Mono-n-butyl phthalate, methylparaben, bisphenol A, and hydroxynaphthalene represented the most abundant mPAE, parabens, bisphenol, and OH-PAH compounds, respectively. The present PAHs are mainly exposed to human through inhalation, while the chemicals added to personal care products are mainly exposed to human through oral intake and dermal contact. The urine samples from suburban subjects showed significantly higher OH-PAH levels than the urine samples from urban subjects, and females had lower OH-PAH levels than males. Urinary concentrations of the analyzed contaminants were significantly correlated with age, body mass index, residence time, as well as the frequencies of alcohol consumption and swimming. Risk assessments based on Monte Carlo simulation indicated that approximately 30% of the subjects suffered non-carcinogenic risks from mPAEs and OH-PAHs, with mPAEs accounting for 89% of the total risk.

Polycyclic aromatic hydrocarbons (PAHs) exposure is associated with heart rate variability (HRV) reduction, a widely used marker of cardiovascular autonomic dysfunction. The role of DNA methylation in the relationship between PAHs exposure and decreased HRV is largely unknown. This study aims to explore epigenome-wide DNA methylation changes associated with PAHs exposure and further evaluate their associations with HRV alternations among non-current smokers. We measured 10 mono-hydroxylated PAHs (OH-PAHs) in urine and DNA methylation levels in blood leukocytes among participants from three panels of Chinese non-current smokers (152 in WHZH, 99 in SY, and 53 in COW). We conducted linear regression analyses between DNA methylation and OH-PAHs metabolites with adjustment for age, gender, body mass index, drinking, blood cell counts, and surrogate variables in each panel separately, and combined the results by using inverse-variance weighted fixed-effect meta-analysis to obtain estimates of effect size. The median value of total OH-PAHs ranged from 0.92 × 10⁻² in SY panel (62.6% men) to 13.82 × 10⁻² μmol/mmol creatinine in COW panel (43.4% men). The results showed that methylation levels of cg18223625 (COL20A1) and cg07805771 (SLC16A1) were significantly or marginally significantly associated with urinary 2-hydroxynaphthalene [β(SE) = 0.431(0.074) and 0.354(0.068), FDR = 0.016 and 0.056, respectively], while methylation level of cg09235308 (PLEC1) was positively associated with urinary total OH-PAHs [β(SE) = 0.478(0.079), FDR = 0.004]. Hypermethylations of cg18223625, cg07805771, and cg09235308 were inversely associated with HRV indices among the WHZH and COW non-current smokers. However, we did not observe significant epigenome-wide associations for the other 9 urinary OH-PAHs. These findings provide new evidence that PAHs exposure is linked to differential DNA methylation, which may help better understand the influences of PAHs exposure on HRV alternations.

Urban environments are characterized by multiple exposures that may influence body mass index (BMI) growth in early life. Previous studies are few, with inconsistent results and no evaluation of simultaneous exposures. Thus, this study aimed to assess the associations between exposure to air pollution, green spaces and built environment characteristics, and BMI growth trajectories from 0 to 5 years. This longitudinal study used data from an electronic primary care health record database in Catalonia (Spain), including 79,992 children born between January 01, 2011 and December 31, 2012 in urban areas and followed until 5 years of age. Height and weight were measured frequently during childhood and BMI (kg/m²) was calculated. Urban exposures were estimated at census tract level and included: air pollution (nitrogen dioxide (NO₂), particulate matter <10 μm (PM₁₀) and <2.5 μm (PM₂.₅₎), green spaces (Normalized Difference Vegetation Index (NDVI) and % green space) and built environment (population density, street connectivity, land use mix, walkability index). Individual BMI trajectories were estimated using linear spline multilevel models with several knot points. In single exposure models, NO₂, PM₁₀, PM₂.₅, and population density were associated with small increases in BMI growth (e.g. β per IQR PM₁₀ increase = 0.023 kg/m², 95%CI: 0.013, 0.033), and NDVI, % of green spaces and land use mix with small reductions in BMI growth (e.g. β per IQR % green spaces increase = −0.015 kg/m², 95%CI: −0.026, −0.005). These associations were strongest during the first two months of life. In multiple exposure models, most associations were attenuated, with only those for PM₁₀ and land use mix remaining statistically significant. This large longitudinal study suggests that early life exposure to air pollution, green space and built environment characteristics may be associated with small changes in BMI growth trajectories during the first years of life, and that it is important to account for multiple exposures in urban settings.

In early nineteen century, a gas field was operational in southern part of Sindh, Pakistan for power production. The plant was completely un-operational for last three decades, whereas all wastage and raw materials are still dumped there, which might be the source to contaminate the ground water. The most of the workers population still living in different villages nearby the gas field. In present study, evaluated the undesirable effects of the toxic metals (lead and cadmium) via consuming groundwater for drinking and other domestic purpose especially in children of ≤5.0 years. For comparative purpose groundwater of nonindustrial area (nonexposed) was also analysed and their impact on age matched children was carried out. Biological samples (scalp hair and blood) were collected from children of exposed and nonexposed areas. The Cd and Pb in scalp hair and blood samples were carried out by graphite furnace atomic absorption spectrometry. Whereas, Cd and Pb in groundwater obtained from both areas were determined prior to applied preconcentration method as reported in our previous works. The Cd and Pb contents in the groundwater of villages of exposed area were found in the range of 5.18–10.9 and 19.9–69.5 μg/L, respectively. Whereas, the groundwater of nonexposed area contains Cd and Pb in the range of 1.79–3.78 and 5.07–24.3 μg/L, respectively. It was observed that the concentrations of Cd and Pb in scalp hair and blood samples of children belongs to exposed area have ≥2.0 fold higher than the resulted data attained for age matched control children, indicating as the exposure biomarkers of toxic metals. The children belong to exposed area have poor health, anemic and low body mass index (<13 kg/m2). A significant positive correlations among Cd and Pb concentrations in biological samples of exposed subjects and groundwater was observed (p < 0.01).

Epidemiological studies have demonstrated association between the total mass of fine particulate matter (PM2.5) exposures and inflammation. There are few studies exploring the associations between PM2.5 constituents and the biomarkers of inflammation in older adults and the underlying biological mechanisms are not exact. In this study, we examined the associations between PM2.5 and its constituents (organic carbon (OC), elemental carbon (EC), total carbon (TC), polycyclic aromatic hydrocarbons (PAHs) and complement three factor (C3), an important biomarker of inflammation in a repeated panel of 175 older adults in Beijing, China. We have constructed three different linear mixed effect models (single-pollutant model, constituent-PM2.5 joint model, and constituent-residual model) to evaluate the association of PM2.5 and its constituents and complement C3, controlling for concentration of high sensitive C-reactive protein (hs-CRP), day of week, mean temperature, relative humidity, location and potential individual confounders. We found robust positive associations of OC, EC, TC, PAHs and PM2.5 mass concentration with complement C3 at different lag patterns. The cumulative effects of pollutants increased across average of 2–5 days. Individuals aged 65 and above, or with diabetes, or BMI ≥30, or with no-cardiopathy, or with hypertension also exhibited positive associations between PM2.5 and complement C3. The results revealed that short-term exposure to PM2.5 and its constituents could result in a significant increase in serum level of complement C3. These findings suggested a possible involvement of complement C3 in the effect of PM2.5 on inflammatory reaction.

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.

Organophosphate esters (OPEs) and phthalate esters (PAEs) are extensively used as additives in commercial and household products. However, knowledge on human exposure to OPEs and PAEs remains limited in China. This study aimed to investigate OPE and PAE metabolites in urine samples of primiparas and to evaluate the cumulative risk of OPE and PAE exposure. A total of 8 OPE metabolites and 11 PAE metabolites were measured in urine samples of 84 primiparas from Shenzhen, China. The OPE metabolites were found in at least 72% of the urine samples with bis(2-chloroethyl) phosphate (BCEP) being the dominant analogue. Among the 11 PAE metabolites, mono-n-butyl phthalate (mBP) was the most abundant analogue and had a median concentration (139 μg/L) greater than those reported in urine samples from other countries and regions. A significant, positive correlation was found between Σ₈OPEMs (the sum of 8 OPE metabolites) and body mass index (BMI). The urinary concentration of Σ₁₁PAEMs (the sum of 11 PAE metabolites) was positively associated with the time of computer using by the primiparas. The estimated daily intakes (EDI) of tris(2-chlorethyl) phosphate (TCEP, the parent chemical of BCEP) and di-n-butyl phthalate (DnBP, the parent chemical of mBP) were determined to be 0.47 and 9.14 μg/kg bw/day, respectively. The 95th percentile EDI values for TCEP and DnBP both exceeded their corresponding reference doses. Twelve and fifty-five percentage of the primiparas were estimated to have HIRfD (hazard index corresponding to reference doses) and HITDI (hazard index corresponding to tolerable daily intake) values exceeding 1 for OPEs and PAEs, respectively, suggesting a relatively high exposure risk.

Organochlorine pesticides (OCPs), including dichlorodiphenyltrichloroethane (DDT) and its metabolites [dichlorodiphenyldichloroethylene (DDE) and dichlorodiphenyldichloroethane], hexachlorocyclohexanes (HCHs), and hexachlorobenzene (HCB), are widely detected in humans despite the considerable decline in environmental concentrations. To understand the placental transfer of OCPs and the possible maternal influence on them, we measured the concentrations of DDTs, HCHs, and HCB in 102 paired samples of maternal and cord sera, and placentas collected in Shanghai, China. The median concentrations of DDTs and HCHs were the highest in maternal sera (601, 188 ng g⁻¹ lipid), followed by umbilical cord sera (389, 131 ng g⁻¹ lipid), and placentas (65, 37 ng g⁻¹ lipid). 4,4′-DDE, β-HCH, and HCB were the predominant contaminants in the three matrices. The ubiquitous existence of OCPs, and the significant concentration relationships of DDTs, HCHs, and OCPs in the three matrices suggested placental transfer from mother to fetus. The lipid-based concentration ratios of 4,4′-DDE, β-HCH, and HCB in umbilical cord serum to those in maternal serum (F/M), and ratios of placenta to maternal serum (P/M) ranged from 0.66 to 1.01, and 0.12 to 0.25, respectively. Maternal variables affected the levels of fetal contamination. For primiparous women, significant correlations between maternal age and maternal HCHs, and between pre-pregnancy body mass index (BMI) and maternal HCHs were found. The negative effect of parity, and the positive effect of food consumption on maternal OCP concentrations were also observed, although there were no significant differences. The possible influence of parity on F/M and P/M of 4,4′-DDE suggested borderline significant differences between primiparous and multiparous women. Also, slight group differences were observed between elder and younger women, and between overweight and normal/underweight women. Parity seems to have a potential influence on transfer ratios of some OCP pollutants.

Parabens, known as ubiquitous preservatives, have been linked to adverse health outcomes in humans. This study aimed to examine urinary paraben concentrations of children at 3 years of age and evaluate their associations with anthropometric parameters. Urinary parabens including methylparaben (MeP), ethylparaben (EtP), propylparaben (PrP), butylparaben (BuP) and benzylparaben (BeP) were measured among 436 children in a birth cohort using gas chromatography with tandem mass spectrometry. Generalized linear models were performed to evaluate associations of paraben exposures with age- and sex-specific z scores, including weight, height, weight for height and body mass index. MeP, EtP and PrP were the dominant parabens in urinary samples, with the median concentrations of 6.03 μg/L, 3.17 μg/L, 2.40 μg/L, respectively. The median values of estimated daily intake (EDIurine) of five urinary paraben concentrations were 12.10, 5.68, 4.50, 0.06 and 0.17 μg/kg-body weight/day, respectively. Urinary EtP concentrations were positively associated with weight z scores [regression coefficient β = 0.16, 95% confidence interval (CI): 0.04, 0.29; p = 0.01] and height z scores (β = 0.15, 95% CI: 0.03, 0.27; p = 0.01). Positive associations were found between the sum of molar concentrations of five parabens and height z scores among all children (β = 0.24, 95% CI: 0.04, 0.45; p = 0.02). These significant associations were only observed in boys. Our findings suggest that exposure to parabens may be adversely associated with physical growth in 3-year-old boy children. Further prospective studies are warranted to understand the toxicological mechanisms of paraben exposures and potential risk of children.