In this study, we evaluated the effects of geo-climatic parameters and other potential risk factors on the prevalence of chronic toxoplasmosis (CT) in pregnant women. We searched PubMed/MEDLINE, Web of Science, EMBASE, Scopus, and SciELO databases for seroepidemiological studies published between January 1988, and February 2021. We performed meta-analysis and meta-regression by using a random effect model to synthesize data. A total of 360 eligible datasets, including 1,289,605 pregnant women from 94 countries, were included in this study. The highest and lowest prevalence rates were estimated for latitudes of 0–10° (49.4%) and ≥50° (26.8%); and for the longitude of 80–90° (44.2%) and 110–120° (7.8%), respectively. Concerning climatic parameters, the highest and lowest prevalence rates were estimated in regions with the mean relative humidities of >80% (46.6%) and <40% (27.0); annual precipitation between 1000 and 1500 mm (39.2%) and 250–500 mm (26.8%); and mean annual temperature of 20–30 °C (36.5%), and <7 °C (24.9%), respectively. Meta-regression analyses indicated significant increasing trends in prevalence of CT in pregnant women with decrease in geographical latitude (coefficient, = −0.0035), and geographical longitudes (C = −0.0017). While it was positively associated (P < 0.01) with the mean environmental temperature (C = 0.0047), annual precipitation (C = 0.000064), and mean relative humidity (C = 0.002). Our results highlighted various effects of environmental parameters on the prevalence of CT. Therefore, different regions in the world may benefit from different types of interventions, and thus, novel preventive measures in a region should be developed according to local climate, agricultural activities and people culture.

Emerging per-/polyfluoroalkyl substances (PFASs), such as chlorinated polyfluorinated ether sulfonates (Cl-PFESAs), have been detected in human samples, yet investigation on their occurrence in pregnant women remains limited. Herein, ten legacy PFASs, branched perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA), two Cl-PFESAs, perfluoro-2-propoxypropanoic acid (HFPO-DA), and ammonium 4,8-dioxa-3H-perfluorononanoate (ADONA) were detected in serum samples from 480 pregnant women in Tianjin, China. The influencing effects of age, body mass index, gravidity, and parity were also evaluated. PFOS [geographic mean (GM): 7.05 ng/mL], 6:2Cl-PFESA (GM: 5.31 ng/mL), and PFOA (GM: 2.82 ng/mL) were the dominant PFASs in the serum of pregnant women, while neither HFPO-DA nor ADONA was detectable in any serum. The serum concentration of Cl-PFESAs and 6:2Cl-PFESA/PFOS ratio in the present study were 2–5 times higher than that in previous studies of pregnant women in China. Serum concentrations of Cl-PFESAs were significantly correlated with all detected PFAAs (Spearman’s Rho: 0.15–0.69, p < 0.01) excepting perfluoropentanesulfonate (PFPeS), indicating common exposure sources for Cl-PFESAs and PFAAs and some particular exposure source for PFPeS. Younger age and multi-parity were associated with lower serum concentrations of PFOS and several perfluoroalkyl sulfonates but not associated with Cl-PFESAs or PFOA, suggesting an increasing exposure to Cl-PFESAs and PFOA which neutralized the impact of age and parity. Overall, this study indicated a relatively high exposure level and composition of 6:2Cl-PFESA in pregnant women in the north coast of China, which highlights the need to investigate the exposure sources in this area.

The influenza is a common viral infection that can be fatal, especially in high-risk groups such as children, pregnant women, elderly, and immune-deficient individuals. Vaccination is the most efficient approach to prevent the spreading of viral infection and promote individual and public health. In contrast, exposure to environmental pollutants such as cigarette smoke reduces the efficacy of vaccination. We investigated whether chronic exposure to hydroquinone (HQ), the most abundant compound of the tobacco particulate phase, could impair the adaptive immune responses elicited by influenza vaccination. For this, adult male C57BL/6 mice were daily exposed to either nebulized HQ or PBS for 1 h for a total of eight weeks. At weeks 6 and 8, the mice were primed and boosted with the trivalent influenza vaccine via IM respectively. Although the HQ exposure did not alter the body weight of the mice and the biochemical and hematological parameters, the pollutant increased the oxidative stress in splenocytes of immunized animals, modified the morphology of spleen follicles, and augmented the size of their lymph nodes. The lymphoid organs of HQ-exposed mice presented a similar number of vaccine-specific IgG-secreting cells, titers of vaccine-specific total IgG, and respective subclasses. Transcriptome studies with HQ, benzene, or cigarette smoke exposure were also analyzed. The genes up-regulated upon pollutant exposure were associated with neutrophil migration and were shown to be co-expressed with antibody-secreting cell genes. Therefore, these findings suggest that HQ exposure may trigger an immune-compensatory mechanism that enhances the humoral responses induced by influenza vaccination.

Bisphenol S (BPS) has been progressively used due to the potential safety problems of bisphenol A (BPA). Thus Human studies are needed to investigate the developmental effects of BPS. In this study, the impact of maternal BPS exposure on birth outcomes was evaluated with linear and logistic regression models. BPS was analyzed in spot urine samples collected from 985 pregnant women at admission to labor. It was found in 93.7% of the urine samples with the specific gravity adjusted geometric mean concentration of 0.17 μg/L. One ln-unit increase in urinary BPS was associated with a 0.72-day increase in pregnancy duration (95% CI: 0.34, 1.09). When stratified by fetal sex, each ln-unit increase in maternal urinary BPS was significantly correlated with increased gestational age [adjusted β = 1.02, 95% confidence intervals (CI): 0.47, 1.57] and increased odds of late term birth [adjusted odds ratio = 1.29, 95% CI: 1.00, 1.67] for girls, but not significantly for boys. Including maternal urinary BPA and BPS in one model did not change the results. Associations of BPS with birth weight or length were not observed. This is the first report about BPS exposure for pregnant women from China. Higher maternal urinary BPS concentrations were associated with increased gestational age, suggesting maternal BPS exposure may interfere with pregnancy duration. The findings require replication but reveal the probable risks posed by the developmental BPS exposure.

Triclosan (TCS) is a suspected endocrine disrupting chemical which is widely used in consumer products as an antibacterial agent. But findings in human studies focusing on the fetal developmental effects of prenatal TCS exposure were rare and inconsistent. This study aimed to determine maternal urinary TCS and investigate its association with birth outcomes. Pregnant women (n = 1006) were randomly selected from the prospective Healthy Baby Cohort (HBC) enrolled in 2014. TCS levels were determined in maternal urine samples collected at delivery and recorded birth outcomes were obtained from the medical records. Multiple linear regressions were applied to evaluate associations of maternal urinary TCS levels with birth outcomes including birth weight, birth length, and gestational age. Logistic regressions were used to evaluate associations with preterm birth, late term birth, and low birth weight. The geometric mean concentrations for TCS and specific gravity (SG) adjusted TCS in maternal urines were 0.73, 0.78 ng/mL, respectively. In the crude model, one ln-unit increase of urinary SG-adjusted TCS concentration was associated with a 0.30-day [95% confidence interval (CI): 0.00, 0.60] increase in gestational age; however, the associations were not statistically significant after adjustment for covariates. No significant associations of SG-adjusted TCS concentrations with birth weight and birth length were observed. Maternal SG-adjusted TCS concentrations were not related to preterm birth, late term birth, and low birth weight (all p > 0.10). Our findings reported a relatively low level of TCS among Chinese pregnant women. With such exposure level, we did not find strong evidence for associations between maternal TCS exposure and birth outcomes. Longitudinal studies concerning about different potential effects of TCS on perinatal health are necessary.

Human exposure to polybrominated diphenyl ethers (PBDEs) has been increasing over the last three decades in China and around the world. Animal studies suggest that PBDEs could reduce blood levels of thyroid hormones, but it is unclear whether PBDEs disrupt thyroid function in humans. We used data from a prospective birth cohort of 123 pregnant women who were enrolled between September 2010 and March 2011 in Shandong, China. We measured the concentrations of eight PBDE congeners (n = 106) and five thyroid hormones (n = 107) in cord serum samples. We examined the relationship between prenatal exposure to PBDEs and thyroid function (n = 90). Median concentrations of BDEs 47, 99, 100, and 153 (detection frequencies > 75%) were 3.96, 8.27, 3.31, and 1.89 ng/g lipid, respectively. A 10-fold increase in BDE-99 and Σ4 PBDEs (the sum of BDEs 47, 99, 100, and 153) concentrations was associated with a 0.41 μg/dL (95% confidence interval [CI]: 0.10 to 0.72) and 0.37 μg/dL (95% CI: 0.06 to 0.68) increase in total thyroxine levels (TT4), respectively. No associations were found between other individual congeners and any of the five thyroid hormones. Our study suggests that prenatal exposure to PBDEs may be associated with higher TT4 in cord blood. Given the inconsistent findings across existing studies, our results need to be confirmed in additional studies.

Evidence supporting an inverse association between maternal exposure to air pollutants and foetal growth has been accumulating. However, the findings from Asian populations are limited, and the question of critical windows of exposure remains unanswered. We examined whether maternal exposure to air pollutants, in particular exposure during the first trimester (an important period of placental development), was associated with foetal growth in Japanese term infants. From the Japan Perinatal Registry Network database, we received birth data for 29,177 term singleton births in western Japan (Kyushu-Okinawa Districts) between 2005 and 2010. Exposure was expressed in terms of average concentrations of air pollutants (ozone, suspended particulate matter, nitrogen dioxide, and sulphur dioxide), as measured at the nearest monitoring stations to the respective delivery hospitals of the pregnant women, during the entire pregnancy and each trimester. As proxy markers of foetal growth restriction, we used small for gestational age (SGA), and adverse birth weight (low birth weight in addition to SGA). For pollutant exposure during the entire pregnancy, we did not observe the association with SGA and adverse birth weight. In the single-trimester model for the first trimester, however, we found a positive association between ozone exposure, and SGA (odds ratio [OR] per 10 ppb increase = 1.07, 95% confidence interval [CI] = 1.01–1.12) and adverse birth weight (OR = 1.07; 95% CI = 1.01–1.14). This association persisted in the multi-trimester model, and no association for exposure during the second or third trimester was observed. Exposure to other pollutants during each trimester was not associated with these outcomes. In conclusion, maternal exposure to ozone during the first trimester was independently associated with an elevated risk of poor foetal growth.

Quantifying population exposure level to tobacco smoke is important for investigating its adverse effects on human health. We aimed to investigate the feasibility and application of using population hair concentrations of nicotine and cotinine to indicate their exposure level to tobacco smoke among pregnant women. Our study recruited 256 mothers who delivered healthy babies and collected their hair samples from scalp, of which 172 mothers were self-reported non-passive smokers and the other 84 mothers were self-reported passive smokers. We analyzed nicotine and cotinine concentrations of the hair section grown during the early pregnancy. The linear relationship between cotinine and nicotine was developed and validated by internal cross-validation method. Our results revealed that self-reported passive smokers had higher concentrations of nicotine [2.08 (1.00–4.46) ng/mg hair, i.e. median value (inter-quartile range)] and cotinine [0.063 (0.041–0.148) ng/mg hair] than non-passive smokers [1.35 (0.58–2.59) ng/mg hair of nicotine and 0.049 (0.022–0.087) ng/mg hair of cotinine, respectively]. There existed a linear regression model between hair cotinine and nicotine concentrations, i.e. [cotinine] = 0.024 × [nicotine]+0.0184 (R2 = 0.756) for this population. The internal cross-validation squared correlation coefficient slightly increased from 0.689 to 0.734 with the training subjects varying from 20% to 90%, suggesting that this regression model had high robustness and predictive accuracy. It was concluded that nicotine in maternal hair can evaluate the hair cotinine level and reflect maternal passive exposure level to ambient tobacco smoke with high sensitivity.

Mercury loads in tropical estuaries are largely controlled by the rainfall regime that may cause biodilution due to increased amounts of organic matter (both live and non-living) in the system. Top predators, as Trichiurus lepturus, reflect the changing mercury bioavailability situations in their muscle tissues. In this work two variables [fish weight (g) and monthly total rainfall (mm)] are presented as being important predictors of total mercury concentration (T-Hg) in fish muscle. These important explanatory variables were identified by a Weibull Regression model, which best fit the dataset. A predictive model using readily available variables as rainfall is important, and can be applied for human and ecological health assessments and decisions. The main contribution will be to further protect vulnerable groups as pregnant women and children. Nature conservation directives could also improve by considering monitoring sample designs that include this hypothesis, helping to establish complete and detailed mercury contamination scenarios.

Exposure to polycyclic aromatic hydrocarbons (PAHs) during pregnancy is a risk factor for adverse neurobehavioral development outcomes. Mitochondrial DNA are sensitive to environmental toxicants due to the limited ability of repairing. The change of mitochondrial DNA copy number (mtDNAcn) might be a biologically mechanism linking PAH exposure and children’s neurobehavioral impairment. Our aims are to explore whether PAH metabolites in maternal urine were associated with children’s neurobehavioral development at 2 years old and umbilical cord blood mtDNAcn, and whether mtDNAcn was a mediator of PAH-related neurobehavioral development. We included 158 non-smoking pregnant women from Taiyuan City, Shanxi Province. Maternal urinary eleven PAH metabolites were detected by high performance liquid chromatography with tandem mass spectrometry (HPLC-MS/MS). MtDNAcn in cord blood was detected by real time quantitative polymerase chain reaction (RT-PCR). Children’s neurodevelopment was measured by Gesell Developmental Schedules (GDS) when children were two years age. Generalized linear models and restricted cubic spline models were applied to assess the relationships between PAH metabolites in maternal urine and GDS scores and mtDNAcn. A mediation analysis was also conducted. Generalized linear models showed the relationships of sum of PAH metabolites (Σ-OHPAHs) in maternal urine with decreased motor score, and Σ-OHPAHs with increased mtDNAcn (p for trend < 0.05). Urinary levels of Ln (Σ-OHPAHs) increased one unit was related to a 2.08 decreased in motor scores, and Ln (Σ-OHPAHs) increased one unit was related to 0.15 increased in mtDNAcn. Mediation analysis did not find mtDNAcn can be a mediator between PAH metabolites and neurobehavioral development. Our results suggest that prenatal exposure to PAH decreased children’s neurobehavioral development scores and increased mtDNAcn. And reducing exposure to PAH during pregnancy will benefit to improving neurobehavioral development in children.In our present cohort study, sum of PAH metabolites in urine of pregnant women were related with motor score and were positively associated with umbilical cord blood mtDNA copy number.