Evidence for effects of PM₂.₅ on systemic oxidative stress in pregnant women is limited, especially in early pregnancy. To estimate the associations between ambient PM₂.₅ exposures and biomarkers of lipid peroxidation and total antioxidant capacity (T-AOC) in women with normal early pregnancy (NEP) and women with clinically recognized early pregnancy loss (CREPL), 206 early pregnant women who had measurements of serum malondialdehyde (MDA) and T-AOC were recruited from a larger case-control study in Tianjin, China from December 2017 to July 2018. Ambient PM₂.₅ concentrations of eight single-day lags exposure time windows before blood collection at the women’s residential addresses were estimated using temporally-adjusted land use regression models. Effects of PM₂.₅ exposures on percentage change in the biomarkers were estimated using multivariable linear regression models adjusted for month, temperature, relative humidity, gestational age and other covariates. Unconstrained distributed lag models were used to estimate net cumulative effects. Increased serum MDA and T-AOC were significantly associated with increases in PM₂.₅ at several lag exposure time windows in both groups. The net effects of each interquartile range increase in PM₂.₅ over the preceding 8 days on MDA were significantly higher (p < 0.001) in CREPL [52% (95% CI: 41%, 62%)] than NEP [22% (95% CI: 9%, 36%)] women. Net effects of each interquartile range increase in PM₂.₅ over the preceding 5 days on T-AOC were significantly lower (p = 0.010) in CREPL [14% (95% CI: 9%, 19%)] than NEP [24% (95% CI: 18%, 29%)] women. Exposure to ambient PM₂.₅ may induce systemic lipid peroxidation and antioxidant response in early pregnant women. More severe lipid peroxidation and insufficient antioxidant capacity associated with PM₂.₅ was found in CREPL women than NEP women. Future studies should focus on mechanisms of individual susceptibility and interventions to reduce PM₂.₅-related oxidative stress in the first trimester.

An increasing number of findings from epidemiological studies support associations between exposure to air pollution and the onset of several diseases, including pulmonary, cardiovascular and neurodegenerative diseases, and malignancies. However, intermediate, and potentially mediating, biological mechanisms associated with exposure to air pollutants are largely unknown. Previous studies on the human exposome have shown that the expression of certain circulating microRNAs (miRNAs), regulators of gene expression, are altered upon exposure to traffic-related air pollutants. In the present study, we investigated the relationship between particulate matter (PM) smaller than 2.5 μm (PM₂.₅), PM₂.₅ absorbance (as a proxy of black carbon and soot), and ultrafine-particles (UFP, smaller than 0.1 μm), measured in healthy volunteers by 24 h personal monitoring (PEM) sessions and global expression levels of peripheral blood miRNAs. The PEM sessions were conducted in four European countries, namely Switzerland (Basel), United Kingdom (Norwich), Italy (Turin), and The Netherlands (Utrecht). miRNAs expression levels were analysed using microarray technology on blood samples from 143 participants. Seven miRNAs, hsa-miR-24-3p, hsa-miR-4454, hsa-miR-4763-3p, hsa-miR-425-5p, hsa-let-7d-5p, hsa-miR-502-5p, and hsa-miR-505-3p were significantly (FDR corrected) expressed in association with PM₂.₅ personal exposure, while no significant association was found between miRNA expression and the other pollutants. The results obtained from this investigation suggest that personal exposure to PM₂.₅ is associated with miRNA expression levels, showing the potential for these circulating miRNAs as novel biomarkers for air pollution health risk assessment.

Adverse health effects of exposure to air pollution have been investigated in many previous studies. However, there is no study available on the association between maternal exposure to air pollution during pregnancy and cord blood lipid profile. This study, based on 150 mother-newborn pairs residing in Sabzevar, Iran (2018), evaluated the association of exposure to ambient air pollution as well as traffic indicators (total street length in different buffers around residential address and distance to major roads) during entire pregnancy with lipid levels cord blood lipid profile. Concentrations of PM₁₀, PM₂.₅, and PM₁ at maternal residential address were estimated using land use regression (LUR) models. We measured triglyceride (TAG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC) levels and TC/HDL-C and TAG/HDL-C ratio in the cord blood samples to characterize their lipid profile. Multiple linear regression models were developed to estimate the association of exposure to air pollution and traffic indicators with cord blood lipid profile controlled for relevant covariates. Higher concentrations of PM₂.₅ and PM₁₀ were associated with higher levels of TAG, TC, HDL-C, TC/HDL-C, and TAG/HDL-C in cord blood samples. Moreover, higher concentration of PM₁ was associated with higher levels of TAG, TC and LDL-C. There was also a positive association between total street length in 100 m buffer around home and serum levels of TC, TAG, LDL-C and TC/HDL ratio (β = 3.73, 95% confidence intervals (CI): 1.76, 5.71; β = 2.75, 95% CI: 0.97, 4.53; β = 1.87, 95% CI: 0.64, 3.09; β = 0.06, 95% CI: 0.01, 0.11, respectively). However, the associations for total street length in larger buffers and distance to major roads were not statistically significant. Our findings support a relationship between exposure to air pollution during pregnancy and increase in cord blood lipid levels.

F–53B and PFOS are two per- and polyfluoroalkyl substances (PFASs) widely utilized in the metal plating industry as mist suppressants. Recent epidemiological studies have linked PFASs to cardiovascular diseases and alterations in heart geometry. However, we still have limited understanding of the effects of F–53B and PFOS on the developing heart. In this study, we employed a human embryonic stem cell (hESC)-based cardiac differentiation system and whole transcriptomics analyses to evaluate the potential developmental cardiac toxicity of F–53B and PFOS. We utilized F–53B and PFOS concentrations of 0.1–60 μM, covering the levels detected in human blood samples. We demonstrated that both F–53B and PFOS inhibited cardiac differentiation and promoted epicardial specification via upregulation of the WNT signaling pathway. Most importantly, the effects of F–53B were more robust than those of PFOS. This was because F–53B treatment disrupted the expression of more genes and led to lower cardiac differentiation efficiency. These findings imply that F–53B may not be a safe replacement for PFOS.

Current studies indicate that long-term exposure to ambient fine particulate matter (PM₂.₅) is related with global mortality, yet no studies have explored relationships of PM₂.₅ and its species with DNAm PhenoAge acceleration (DNAmPhenoAccel), a new epigenetic biomarker of phenotypic age. We identified which PM₂.₅ species had association with DNAmPhenoAccel in a one-year exposure window in a longitudinal cohort. We collected whole blood samples from 683 elderly men in the Normative Aging Study between 1999 and 2013 (n = 1254 visits). DNAm PhenoAge was calculated using 513 CpGs retrieved from the Illumina Infinium HumanMethylation450 BeadChip. Daily concentrations of PM₂.₅ species were measured at a fixed air-quality monitoring site and one-year moving averages were computed. Linear mixed-effect (LME) regression and Bayesian kernel machine (BKM) regression were used to estimate the associations. The covariates included chronological age, body mass index (BMI), cigarette pack years, smoking status, estimated cell types, batch effects etc. Benjamini-Hochberg false discovery rate at a 5% false positive threshold was used to adjust for multiple comparison. During the study period, the mean DNAm PhenoAge and chronological age in our subjects were 68 and 73 years old, respectively. Using LME model, only lead and calcium were significantly associated with DNAmPhenoAccel. For example, an interquartile range (IQR, 0.0011 μg/m³) increase in lead was associated with a 1.29-year [95% confidence interval (CI): 0.47, 2.11] increase in DNAmPhenoAccel. Using BKM model, we selected PM₂.₅, lead, and silicon to be predictors for DNAmPhenoAccel. A subsequent LME model showed that only lead had significant effect on DNAmPhenoAccel: 1.45-year (95% CI: 0.46, 2.46) increase in DNAmPhenoAccel following an IQR increase in one-year lead. This is the first study that investigates long-term effects of PM₂.₅ components on DNAmPhenoAccel. The results demonstrate that lead and calcium contained in PM₂.₅ was robustly associated with DNAmPhenoAccel.

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).

In Brazil, there are scarce data on lead (Pb) and cadmium (Cd) contamination, especially for more vulnerable populations such as preschool children. In this paper, we answer two questions: (1) What are the exposure levels of lead and cadmium in preschool children, in Sao Paulo, Brazil? and (2) What are the risk factors associated with this exposure? This cross-sectional study included 50 day care centers (DCCs), totaling 2463 children aged 1–4 years. Venous blood samples were analyzed by ICP-MS. Questionnaires were administered to the parents. Multiple logistic regression models were used to identify associations between blood lead levels (BLLs) and blood cadmium levels (BCLs) and potential risk factors. The geometric mean for BLLs was 2.16 μg/dL (95% CI: 2.10–2.22 μg/dL), and the 97.5th percentile was 13.9 μg/dL (95% CI: 10.0–17.3 μg/dL). For cadmium exposure, the geometric mean for BCLs was 0.48 μg/L (95% CI: 0.47–0.50 μg/L), and the 95th percentile was 2.57 μg/L (95% CI: 2.26–2.75 μg/L). The DCCs’ geographic region was associated with high BLLs and BCLs, indicating hot spots for lead and cadmium exposures. In addition, it was found that the higher the vehicles flow, the higher were the BLLs in children. Red lead in household gates was also an important risk factor for lead exposure. Comparing these results with the findings of the Fourth National Report on Human Exposure to Environmental Chemicals by CDC-2013, it was found that in Brazilian preschool children the BLLs are almost three times higher (97.5th percentile) and the BCLs are almost twelve times higher (95th percentile) than those in U.S. children. This information is essential to formulate public health policies.

The Qinling subspecies of giant panda (Ailuropoda melanoleuca qinlingensis), is highly endangered; fewer than 350 individuals still inhabit Qinling Mountains. Previous research revealed captive pandas were exposed to bromine, so we hypothesized that captive pandas were exposed to and affected by polybrominated diphenyl ethers (PBDEs). To test this hypothesis, we tested blood and feces of captive and wild pandas, their drinking water, food (bamboo leaves) from SWARC (Shaanxi Wild Animal Research Center)and FNNR (Foping National Nature Reserve) and supplemental feedstuff given to captive panda at SWARC. We found 13 congeners of PBDEs in fecal samples, of which BDE47, BDE66, BDE71, BDE99, and BDE154 were the dominant, total PBDE concentration in feces of captive pandas was 255% higher than in wild pandas. We found nine PBDEs congeners in blood samples: BDE153 and BDE183 were the predominant congers. PBDEs in blood from captive pandas were significantly higher than in wild pandas. The total concentration of PBDEs were 5473 and 4835 (pg.g) in Fargesia qinlingensis, were 2192 and 1414 (pg.g) in Bashannia fargesii (2192, 1414 pg g), 0.066, 0.038 (pg/ml) in drinking water, and 28.8 (pg.g) in supplemental feedstuff for captive and wild pandas, which indicate that the PBDEs came from its bamboo feed, especially from Bashannia fargesii. Our results demonstrate that BDE99 and BDE47 could be threatening the pandas’ health especially for captive panda and there are potential health risks from PBDEs for pandas. In the short term, this risk may be ameliorated by strict control of food quality. In the long term, however, reducing air, water and soil contamination so as to improve environmental quality can best reduce these risks to meet the international standard such as Stockholm Convention.

In Yucatan, Mexico, chronic exposure of Mayan population to pesticides is expected as about 30 per cent are drinking polluted water. Residues of organochlorine pesticides (OCP) were monitored in 18 municipalities of Yucatan with high mortality rates due to uterine cervix cancer. 70 blood samples collected from Mayan women living in livestock, agricultural and metropolitan area were analyzed for OCP. Solid Phase Extraction was performed on C18 cartridges and analyzed by Gas Chromatography with Electron Capture Detector. The results showed that the highest OCP levels were detected in blood of women living in the livestock area. OCP detected were endosulfan I (7.35 μg/mL), aldrin (3.69 μg/mL), 4,4′ DDD (2.33 μg/mL), 1.39 and 1.46 μg/mL of δ-HCH. Women from the agricultural area had high concentrations of OCP in their blood, particularly dieldrin (1.19 μg/mL), and 1.26 μg/mL of 4,4′ DDE. In the metropolitan area, 0.080 μg/mL of γ-HCH and 0.064 μg/mL of heptachlore were detected. This monitoring study was also based on epidemiological data of uterine cervical cancer. It was found that environmental factors may have facilitated the infiltration of OCP to the aquifer used for potable water supply. These factors in addition to poverty can have impacts on public health. This first exploratory study suggests that monitoring of OCP in human is important for the establishment of health promotion programs. The integrative analysis of both, environmental and social factors would be helpful to characterize the bioaccumulation of pesticides in humans.

As a highly toxic heavy metal, the pollution and exposure risks of lead are of widespread concern for human health. However, the collection of blood samples for use as an indicator of lead pollution is not always feasible in most cohort or longitudinal studies, especially those involving children health. To evaluate the potential use of urinary lead as an indicator of exposure levels and source apportionment, accompanying with environmental media samples, lead concentrations and isotopic measurements (expressed as 207Pb/206Pb, 208Pb/206Pb and 204Pb/206Pb) were investigated and compared between blood and urine from children living in the vicinities of a typical coking plant and lead-acid battery factory. The results showed urinary lead might not be a preferable proxy for estimating blood lead levels. Fortunately, urinary lead isotopic measurements could be used as an alternative for identifying the sources of children's lead exposure, which coincided well with the blood lead isotope ratio analysis.