The presence of polycyclic aromatic hydrocarbons (PAHs) in the fetal environment is a high-priority concern due to the fetus being more sensitive than adults to these ubiquitous xenobiotics. The aim of the present study was to compare the maternal and fetal serum levels of ΣPAHs and their effects on fetal growth in an industrial and an urban area in Southwest Iran. The industrial area was the petrochemical and gas area (PGA) of the Central District of Asaluyeh County and the urban area (UA) was the Central District of Bushehr County, Ninety-nine maternal serum (MS) and 99 cord serum (CS) samples from the PGA and 100 MS and 100 CS samples from the UA were collected during May 2018 to February 2019. The mean concentrations of ΣPAHs were significantly (p < 0.05) higher in the PGA than the UA in both MS (157.71 vs. 93.56 μg/L) and CS (155.28 vs. 93.19 μg/L) samples. Naphthalene (NAP) was the predominant PAH detected in all the studied samples. Significant negative associations were found between birth weight and anthracene (ANT) level in MS (β = −22.917, p = 0.032; weight decrement = 22.917 g for a 1 μg/L increase in ANT); head circumference and chrysene (CHR) level in MS (β = −0.206, p = 0.023; head circumference decrement = 0.206 cm for a 1 μg/L increase in CHR); and birth height and NAP level in CS (β = −0.20, p = 0.005; height decrement = 0.20 cm for a 1 μg/L increase in NAP). Maternal diet had a significant effect on the serum levels of PAHs. The results of this study showed that transmission of PAHs from mother to fetus through the cord blood is an important issue and mothers who live in industrial areas and consume PAH-containing foodstuffs, and their fetuses, are more at risk than those living in a non-industrial urban area.

Prenatal disinfection by-products (DBPs) exposure is linked with adverse birth outcomes. Genetic susceptibility to DBP metabolism may modify the exposure-outcome associations.To investigate whether CYP2E1 and GSTZ1 genetic polymorphisms modified the associations of prenatal DBP exposures with adverse birth outcomes.Two biomarkers of DBP exposures including trihalomethanes (THMs) in blood and trichloroacetic acid (TCAA) in urine were determined among 426 pregnant women from a Chinese cohort study. CYP2E1 (rs2031920, rs3813867, and rs915906) and GSTZ1 (rs7975) polymorphisms in cord blood were genotyped. Statistical interactions between prenatal DBP exposures and newborns CYP2E1 and GSTZ1 polymorphisms on birth outcomes (birth weight, birth length, and gestational age) were examined by multivariable linear regression with adjustment for potential confounders.We found that newborns CYP2E1 genetic polymorphisms (rs2031920 and rs3813867) modified the associations of maternal blood THMs or urinary TCAA levels with birth outcomes. However, these interactions were nonsignificant after Bonferroni correction for multiple comparisons, except for the interaction between maternal blood BrTHMs [sum of dibromochloromethane (DBCM), bromodichloromethane (BDCM), and bromoform (TBM)] and newborns CYP2E1 gene rs2031920 polymorphisms on birth weight (P for interaction = 0.003).Newborns genetic variations of CYP2E1 rs2031920 may modify the impacts of prenatal BrTHM exposure on birth weight. This finding needs to be further confirmed.

This study aimed to examine the potential association between maternal PBDEs and birth outcomes, including birth weight (g), length (cm), head circumference (cm) and gestational age (week). 215 mothers were recruited from a prospective birth cohort in rural northern China between September 2010 and February 2012. Serum PBDE congeners were detected and their association with birth outcomes were examined. The median maternal serum concentrations of BDE-28, -47, -99, -100, -153 were 2.27, 2.26, 3.58, 2.13, 4.87 ng/g lipid, respectively. Maternal LgBDE-28 and LgBDE-100 were negatively associated with birth length (β = −0.92, 95% confidence interval (CI): −1.82, −0.02; β = −0.97, 95% CI: −1.83, −0.08). A negative association was found between LgBDE-28 and birth weight among male infants (β = −253.76, 95% CI: −438.16, −69.36). PBDE congeners were not associated with head circumference, or gestational age. Our results contribute to growing evidence suggesting that PBDEs have adverse effects on birth outcomes.

Data concerning the effects of prenatal exposures to nonylphenol (NP) and oxidative stress on neonatal birth outcomes from human studies are limited. A total of 146 pregnant women were studied (1) to investigate the association between prenatal NP exposure and maternal oxidative/nitrative stress biomarkers of DNA damage (8-hydroxy-2’-deoxyguanosine (8-OHdG), 8-nitroguanine (8-NO2Gua)) and lipid peroxidation (8-iso-prostaglandin F2α (8-isoPF2α), 4-hydroxy-2-nonenal-mercapturic acid (HNE-MA)) and (2) to explore the associations among oxidative stress biomarkers, NP exposure, and neonatal birth outcomes, including gestational age, birth weight, length, Ponderal index, and head and chest circumferences. NP significantly increased the 8-OHdG and 8-NO2Gua levels. All infants born to mothers with urinary 8-OHdG levels above the median exhibited a significantly shorter gestational duration (Badjusted = −4.72 days; 95% CI: −8.08 to −1.36 days). No clear association was found between NP levels and birth outcomes. Prenatal 8-OHdG levels might be a novel biomarker for monitoring fetal health related to NP exposure.

Perfluorooctane sulfonic acid (PFOS) is a ubiquitous environmental pollutant. In humans, PFOS exposure has been associated with a number of adverse health outcomes, including reduced birth weight. Whether PFOS is capable of affecting angiogenesis and thus possibly fetal development is unknown. Therefore, we investigated 1) the metabolic activity of PFOS-exposed endothelial cells (human umbilical vein endothelial cells, HUVECs), fibroblasts (normal colon fibroblasts, NCFs), and epithelial cells (human colorectal carcinoma cells, HCT116), 2) PFOS-specific inhibition of vascular endothelial growth factor receptor (VEGFR)2 stimulation in KDR/NFAT-RE HEK293 cells, and 3) the antiangiogenic potential of PFOS in a 3D in vitro angiogenesis model of HUVECs and NCFs. In terms of metabolic activity, endothelial cells (HUVECs) were much more sensitive to PFOS than fibroblasts (NCFs) or epithelial cells (HCT116). VEGFR2 signaling in KDR/NFAT-RE HEK293 cells decreased with increasing PFOS concentrations. In co-culture (angiogenesis assay), PFOS treatment resulted in a dose-dependent reduction in tip and branch formation, tip length (μm), and total structural area (μm²) with stable metabolic activity of HUVECs up to high concentrations. We conclude that PFOS possesses antiangiogenic properties. Inhibition of VEGFR2 signaling indicates a possible mechanism of action that can be linked to an existing Adverse Outcome Pathway (AOP43) containing the AO reduced birth weight. Further studies are needed to confirm PFOS-specific adverse effects on angiogenesis, placental perfusion, and fetal growth.

Per- and polyfluoroalkyl substances (PFAS) have been produced and used in a broad range of products since the 1950s. This class, comprising of thousands of chemicals, have been used in many different products ranging from firefighting foam to personal care products and clothes. Even at relatively low levels of exposure, PFAS have been linked to various health effects in humans such as lower birth weight, increased serum cholesterol levels, and reduced antibody response to vaccination. Human biomonitoring data demonstrates ubiquitous exposure to PFAS across all age groups. This has been attributed to PFAS-contaminated water and dietary intake, as well as inadvertent ingestion of indoor dust for adults and toddlers. In utero exposure and breast milk have been indicated as important exposure pathways for foetuses and nursing infants. More recently, PFAS have been identified in a wide range of products, many of which come in contact with skin (e.g., cosmetics and fabrics). Despite this, few studies have evaluated dermal uptake as a possible route for human exposure and little is known about the dermal absorption potential of different PFAS. This article critically investigates the current state-of-knowledge on human exposure to PFAS, highlighting the lack of dermal exposure data. Additionally, the different approaches for dermal uptake assessment studies are discussed and the available literature on human dermal absorption of PFAS is critically reviewed and compared to other halogenated contaminants, e.g., brominated flame retardants and its implications for dermal exposure to PFAS. Finally, the urgent need for dermal permeation and uptake studies for a wide range of PFAS and their precursors is highlighted and recommendations for future research to advance the current understanding of human dermal exposure to PFAS are discussed.

Ambient carbon monoxide (CO) and particulate matters (PMs) are two important air pollutants in urban areas with known impacts on fetuses. Hence, this study measured some biochemistry factors of 200 neonates with birth dates from January 19 to October 12, 2020, including the birth weight and height and the serum levels of ALT, AST, ALP, GGT, and TSH. The Support Vector Machine-fitted land-use regression approach was used to predict the spatio-temporal variability of intra-urban PM 2.5 and CO concentrations by month during the pregnancy period of the cases employing 5 variables of Digital Elevation Model (DEM), slope, and distance from Compressed Natural Gas (CNG) stations, Bus Rapid Transit (BRT) stations, and mines and industries. Spearman correlation analysis (p < 0.05) was performed between the neonate indices and mean monthly PM 2.5 and CO concentrations at the exact residential address of maternal cases and their nearby areas in 250, 500, 1000, 1500, and 2000 m-radius buffer rings. All modeling efforts succeeded in predicting CO and PM 2.5 levels with acceptable adjusted r² values. Northern Isfahan had relatively higher CO and PM 2.5 concentrations due to its adjacency to low-vegetated open lands and its high traffic load as compared to southern areas. The correlation results between the neonate biochemistry indices and mean PM 2.5 and CO concentrations were mostly positive in most buffer rings, especially in the >500 m-radius buffer rings for PM 2.5 and in the 2000 m-radius rings for CO. Although the correlation results of PM 2.5 followed a detectable trend in the buffer rings, the associations between CO and the neonate biochemistry indices differed significantly between the buffer rings. Results showed that increasing mean monthly concentration of CO and PM 2.5 may stimulate further production of liver enzymes while decreasing the birth weight and height.

In most cases, honey bees experience pesticide pollution in a long-term period through direct or indirect exposure, such as the development process from larvae to the pre-harvest stage. At present, little is known about how honey bees respond to pesticide stresses during the continuous development period. This study aims to examine effects of long-term acetamiprid exposure on the development and survival of honey bees, and further present the expression profile in larvae, 1-day-old, and 7-day-old adult worker bees that related to immune, detoxification, acetylcholinesterase (AChE) and memory. Honey bees from 2-day-old larvae to 14-day-old adults except the pupal stage were continuously fed with different acetamiprid solutions (0, 5, and 25 mg/L). We found that acetamiprid over 5 mg/L disturbed the development involving birth weight and emergence rate of newly emerged bees, and reduced the proportion of capped cells of larvae at 25 mg/L; gene expression related to immune and detoxification of worker bees exposed to acetamiprid was roughly activated, returned and then inhibited from larval to emerged and to the late adult stage, respectively. Moreover, lifespans of bees treated with acetamiprid at 25 mg/L were significantly reduced. The present study reflects the potential risk for honey bees continuously exposed to acetamiprid in the development stage.

Previous epidemiological studies have indicated that prenatal exposure to individual metals affect fetal growth. However, the ordinary linear regression has not enough power to assess the mixture effect of multiple metals and cannot capture the possible differences in associations of metal exposures by subgroups of infant birth weight distribution. To investigate the associations of prenatal exposure to metal mixtures with birth weight, and further to assess whether the sensibilities to metal toxicity are dissimilar among infants with poor and normal fetal growth. A total of 16 metals were analyzed in 736 cord samples from a Chinese birth cohort study. Weighted quantile sum regression (WQSR) found the estimate of the metal mixtures was negatively related to birthweight z-score overall [β (95% CI): −0.31 (−0.42, −0.20)], and the major contributors to the mixture index were Cu (39.7%), Ni (18.3%), Mn (14.0%), and Cd (13.1%). Quantile regression showed stronger relations in the tails of birthweight z-score distribution [e.g. the associations of Cu at specific birth weight z-score quantiles were: 10th percentile −0.70 (95% CI: −1.06, −0.35), the 90th percentile −0.35 (95% CI: −0.63, −0.06)]. Our study found that prenatal exposure to Cu, Mn, Ni, and Cd were negatively linked with birthweight z-score. The associations observed were stronger in the tails of birth weight z-score distribution.

Observational studies have indicated that low-to-moderate exposure to cadmium (Cd), lead (Pb), and mercury (Hg) adversely affects birth anthropometry, but results are inconclusive. The aim of this study was to elucidate potential impact on birth anthropometry of exposure to Cd, Pb, and Hg in pregnant women, and to identify the main dietary sources. In the NICE (Nutritional impact on Immunological maturation during Childhood in relation to the Environment) birth-cohort in northern Sweden, blood and urine were collected from pregnant women in early third trimester. Cd, Pb and Hg were measured in erythrocytes (n = 584), and Cd also in urine (n = 581), by inductively coupled plasma mass spectrometry. Dietary data were collected through a semi-quantitative food frequency questionnaire administered in mid-third trimester. Birth anthropometry data were extracted from hospital records. In multivariable-adjusted spline regression models, a doubling of maternal erythrocyte Cd (median: 0.29 μg/kg) above the spline knot of 0.50 μg/kg was associated with reduced birth weight (B: −191 g; 95% CI: −315, −68) and length (−0.67 cm; −1.2, −0.14). The association with birth weight remained when the analysis was restricted to never-smokers. Likewise, a doubling of erythrocyte Hg (median 1.5 μg/kg, mainly MeHg) above 1.0 μg/kg, was associated with decreased birth weight (−59 g; −115, −3.0), and length (−0.29 cm; −0.54, −0.047). Maternal Pb (median 11 μg/kg) was unrelated to birth weight and length. Erythrocyte Cd was primarily associated with intake of plant derived foods, Pb with game meat, tea and coffee, and Hg with fish. The results indicated that low-level maternal Cd and Hg exposure were associated with poorer birth anthropometry. Further prospective studies in low-level exposed populations are warranted.