Association between gestational arsenic exposure and infant physical development: a prospective cohort study.

BACKGROUND: Arsenic pollution is widespread worldwide. The association between gestational arsenic exposure and adverse birth outcomes has been demonstrated in previous studies; however, few investigations have examined whether gestational arsenic exposure has adverse effects on infant growth and development after birth. OBJECTIVE: Our study was designed to evaluate particular associations between gestational arsenic exposure during pregnancy and newborn birth size and to investigate whether these associations continue to affect infants after birth. METHODS: An ongoing prospective cohort study of 1100 pregnant women was conducted at the Wuxi Maternity and Child Health Care Hospital. The total urinary arsenic concentrations in the 2nd and 3rd trimester were determined using atomic fluorescence spectrometry. The relationships between urinary arsenic concentration and foetal growth parameters (birth weight, head circumference, length, and ponderal index), SGA (Small for gestational age), and physical growth of infants within one year after birth were analysed. RESULTS: Urinary arsenic concentration in the 3rd trimester was associated with an increased incidence of SGA [adjusted model: OR = 2.860 (95% CI: 1.168, 7.020), P = 0.021)]. Arsenic exposure in late pregnancy had an adverse effect on the physical development of infants before the age of 1 year, and there was an interaction effect with the sex of infants. The weight and length of boys at 6 and 12 months negatively correlated with maternal urinary arsenic levels during late pregnancy. CONCLUSIONS: In addition to affecting foetal growth, exposure to arsenic in the 3rd trimester also negatively affected the growth of offspring within the first year of life.

Urinary polycyclic aromatic hydrocarbon metabolites and their association with oxidative stress among pregnant women in Los Angeles.

BACKGROUND: Polycyclic aromatic hydrocarbons (PAHs) have been linked to adverse birth outcomes that have been reported to be induced by oxidative stress, but few epidemiological studies to date have evaluated associations between urinary PAH metabolites and oxidative stress biomarkers in pregnancy and identified critical periods for these outcomes and PAH exposures in pregnancy. METHODS: A cohort of pregnant women was recruited early in pregnancy from antenatal clinics at the University of California Los Angeles during 2016-2019. We collected urine samples up to three times during pregnancy in a total of 159 women enrolled in the cohort. A total of 7 PAH metabolites and 2 oxidative stress biomarkers [malondialdehyde (MDA), 8-hydroxy-2'-deoxyguanosine (8-OHdG)] were measured in all available urine samples. Using multiple linear regression models, we estimated the percentage change (%) and 95% confidence interval (CI) in 8-OHdG and MDA measured at each sample collection time per doubling of PAH metabolite concentrations. Furthermore, we used linear mixed models with a random intercept for participant to estimate the associations between PAH metabolite and oxidative stress biomarker concentrations across multiple time points in pregnancy. RESULTS: Most PAH metabolites were positively associated with both urinary oxidative stress biomarkers, MDA and 8-OHdG, with stronger associations in early and late pregnancy. A doubling of each urinary PAH metabolite concentration increased MDA concentrations by 5.8-41.1% and 8-OHdG concentrations by 13.8-49.7%. Linear mixed model results were consistent with those from linear regression models for each gestational sampling period. CONCLUSION: Urinary PAH metabolites are associated with increases in oxidative stress biomarkers during pregnancy, especially in early and late pregnancy.

The impact of PM2.5 and its constituents on gestational diabetes mellitus: a retrospective cohort study.

BACKGROUND: There is increasing evidence that exposure to PM2.5 and its constituents is associated with an increased risk of gestational diabetes mellitus (GDM), but studies on the relationship between exposure to PM2.5 constituents and the risk of GDM are still limited. METHODS: A total of 17,855 pregnant women in Guangzhou were recruited for this retrospective cohort study, and the time-varying average concentration method was used to estimate individual exposure to PM2.5 and its constituents during pregnancy. Logistic regression was used to assess the relationship between exposure to PM2.5 and its constituents and the risk of GDM, and the expected inflection point between exposure to PM2.5 and its constituents and the risk of GDM was estimated using logistic regression combined with restricted cubic spline curves. Stratified analyses and interaction tests were performed. RESULTS: After adjustment for confounders, exposure to PM2.5 and its constituents (NO3-, NH4+, and OM) was positively associated with the risk of GDM during pregnancy, especially when exposure to NO3- and NH4+ occurred in the first to second trimester, with each interquartile range increase the risk of GDM by 20.2% (95% CI: 1.118-1.293) and 18.2% (95% CI. 1.107-1.263), respectively. The lowest inflection points between PM2.5, SO42-, NO3-, NH4+, OM, and BC concentrations and GDM risk throughout the gestation period were 18.96, 5.80, 3.22, 2.67, 4.77 and 0.97 µg/m3, respectively. In the first trimester, an age interaction effect between exposure to SO42-, OM, and BC and the risk of GDM was observed. CONCLUSIONS: This study demonstrates a positive association between exposure to PM2.5 and its constituents and the risk of GDM. Specifically, exposure to NO3-, NH4+, and OM was particularly associated with an increased risk of GDM. The present study contributes to a better understanding of the effects of exposure to PM2.5 and its constituents on the risk of GDM.

Associations between PM2.5, ambient heat exposure and congenital hydronephrosis in southeastern China.

Objectives: This research aims to analyze how exposure to fine particulate matter (PM2.5) and ambient heat during pregnancy increases the risk of congenital hydronephrosis (CH) in newborns. Methods: A case-control study was conducted to investigate the relationship between exposure to PM2.5 and ambient heat during pregnancy and the occurrence of CH in newborns. The study, which was conducted from 2015 to 2020, included 409 infants with CH as the case group and 409 infants without any abnormalities as the control group. Using spatial remote sensing technology, the exposure of each pregnant mother to PM2.5 concentration was meticulously mapped. Additionally, data on the ambient temperature of exposure for each participant were also collected. A logistics regression model was used to calculate the influence of exposure to PM2.5 and ambient heat on the occurrence of CH. Stratified analysis and interaction analysis were used to study the interaction between ambient heat exposure and PM2.5 on the occurrence of CH. Results: At the 6th week of gestation, exposure to PM2.5 may increase the risk of CH. For every 10 µg/m3 increase in PM2.5 exposure, the risk of CH increased by 2% (95%CI = 0.98, 1.05) at a p-value of >0.05, indicating that there was no significant relationship between the results. Exposure to intense heat at 6th and 7th weeks of gestation increased the risk of CH. Specifically, for every 1°C increase in heat exposure, the risk of CH in offspring increased by 21% (95%CI = 1.04, 1.41) during the 6th week and 13% during the 7th week (95%CI = 1.02, 1.24). At 5th and 6th weeks of gestation, the relative excess risk due to interaction (RERI) was greater than 0 at the 50th percentile (22.58°C), 75th percentile (27.25°C), and 90th percentile (29.13°C) of daily maximum temperature (Tmax) distribution, indicating that the risk of CH was higher when exposed to both ambient heat and PM2.5 at the same time compared to exposure to a single risk factor. Conclusion: Exposure to higher levels of PM2.5 and ambient heat during pregnancy increases the risk of CH in infants. There was a positive interaction between exposure to intense heat and high concentration of PM2.5 on the occurrence of CH.

Exposures to non-therapeutic chemicals before, during and after pregnancy: data from the Swiss Teratogen Information Service (STIS).

AIMS OF THE STUDY: Limited knowledge exists regarding exposures to non-therapeutic chemicals by women planning to conceive, or during pregnancy or breastfeeding. The Swiss Teratogen Information Service (STIS) provides information to healthcare professionals about medications and other exposures during pregnancy or breastfeeding. This study aimed to describe the queries on non-therapeutic chemicals addressed to the STIS over the past two decades. METHODS: Using data from the STIS for the years 2000 to 2019, we conducted a descriptive analysis of all queries related to women's exposures to non-therapeutic chemicals during pregnancy planning, pregnancy or breastfeeding. RESULTS: Over two decades, the STIS database recorded 320 exposures to chemicals. Workplace settings accounted for over 60% of queries, followed by exposures at home (20%). In almost half (48%) of the queries, more than one chemical was mentioned, totalling 885 chemicals across these 320 queries. Commonly mentioned chemicals included isopropanol, acetone and lead. Solvents were the leading category of products (16%), followed by cleaning products (10%), paints (8%) and insecticides (5%). The follow-up data showed five diverse cases of congenital malformations, accounting for 4.0% (5 out of 125) of the sample, a figure in line with the background risk of malformations in the general population. CONCLUSIONS: This study emphasises the importance of conducting research that comprehensively captures the highly heterogeneous exposures to non-therapeutic chemicals during pregnancy and suggests that attention should be given not only to professional settings, but also to domestic contexts.

The association of adverse birth outcomes with flood exposure before and during pregnancy in Australia: a cohort study.

BACKGROUND: Exposure to floods might increase the risks of adverse birth outcomes. However, the current evidence is scarce, inconsistent, and has knowledge gaps. This study aims to estimate the associations of flood exposure before and during pregnancy with adverse birth outcomes and to identify susceptible exposure windows and effect modifiers. METHODS: In this cohort study, we obtained all the birth records occurring in Greater Sydney, Australia, from Jan 1, 2001, to Dec 31, 2020, from the New South Wales Midwives Data Collection and in the Brisbane metropolitan region, Australia, from Jan 1, 1995, to Dec 31, 2014, from the Queensland Health Perinatal Data Collection. For each birth, residential address and historical flood information from the Dartmouth Flood Observatory were used to estimate the numbers of days with floods during five exposure windows (Pre-1 was defined as 13-24 weeks before the last menstrual period [LMP], Pre-2 was 0-12 weeks before the LMP, trimester 1 [Tri-1] was 0-12 weeks after the LMP, trimester 2 [Tri-2] was 13-28 weeks after the LMP, and trimester 3 [Tri-3] was ≥29 weeks after the LMP). We estimated the hazard ratios (HRs) of adverse birth outcomes (preterm births, stillbirths, term low birthweight [TLBW], and small for gestational age [SGA]) associated with flood exposures in the five exposure windows using Cox proportional hazards regression models. FINDINGS: 1 338 314 birth records were included in our analyses, which included 91 851 (6·9%) preterm births, 9831 (0·7%) stillbirths, 25 567 (1·9%) TLBW, and 108 658 (8·1%) SGA. Flood exposure in Pre-1 was associated with increased risks of TLBW (HR 1·06 [95% CI 1·01-1·12]) and SGA (1·04 [1·01-1·06]); flood exposure during Tri-1 was associated with increased risks of preterm births (1·03 [1·002-1·05]), stillbirth (1·11 [1·03-1·20]), and SGA (1·03 [1·01-1·06]). In contrast, flood exposures during Pre-2 and Tri-3 were associated with reduced risks. INTERPRETATION: Exposures to floods in Pre-1 and Tri-1 are both associated with increased risks of adverse birth outcomes, and the risks increase with a higher exposure. Upon planning for conception and prenatal care, individuals and health practitioners should raise awareness of the increased risks of adverse birth outcomes after experiencing floods. FUNDING: The Australian Research Council and the Australian National Health and Medical Research Council.

Exploring the association between atmospheric pollutants and preterm birth risk in a river valley city.

Objective: To investigate the association between exposure to atmospheric pollutants and preterm birth in a river valley-type city and its critical exposure windows. Methods: A retrospective cohort study was used to collect data from the medical records of preterm and full-term deliveries in two hospitals in urban areas of a typical river valley-type city from January 2018 to December 2019. A total of 7,288 cases were included in the study with general information such as pregnancy times, the number of cesarean sections, occupation, season of conception and regularity of the menstrual cycle. And confounding factors affecting preterm birth were inferred using the chi-square test. The effects of exposure to each pollutant, including particulate matter 2.5 (PM2.5), particulate matter 10 (PM10), nitrogen dioxide (NO2), sulfur dioxide (SO2), carbon monoxide (CO) and ozone (O3), during pregnancy on preterm birth and the main exposure windows were explored by establishing a logistic regression model with pollutants introduced as continuous variables. Results: Maternal age, pregnancy times, number of births, number of cesarean sections, season of conception, complications diseases, comorbidities diseases, hypertension disorder of pregnancy and neonatal low birth weight of the newborn were significantly different between preterm and term pregnant women. Logistic regression analysis after adjusting for the above confounders showed that the risk of preterm birth increases by 0.9, 0.6, 2.4% in T2 and by 1.0, 0.9, 2.5% in T3 for each 10 µg/m3 increase in PM2.5, PM10, NO2 concentrations, respectively. The risk of preterm birth increases by 4.3% in T2 for each 10 µg/m3 increase in SO2 concentrations. The risk of preterm birth increases by 123.5% in T2 and increases by 188.5% in T3 for each 10 mg/m3 increase in CO concentrations. Conclusion: Maternal exposure to PM2.5, PM10, NO2, CO was associated with increased risk on preterm birth in mid-pregnancy (T2) and late pregnancy (T3), SO2 exposure was associated with increased risk on preterm birth in mid-pregnancy (T2).

Association Between Particulate Matter Exposure and Preterm Birth in Women With Abnormal Preconception Thyrotropin Levels: Large Cohort Study.

Background: Prior research has linked exposure to particulate matter with an aerodynamic diameter of ≤2.5 µm (PM2.5) with preterm birth (PTB). However, the modulating effect of preconception thyroid stimulating hormone (TSH) levels on the relationship between PM2.5 exposure and PTB has not been investigated. Objective: This study aimed to assess whether preconception TSH levels modulate the impact of PM2.5 exposure on PTB. Methods: This cohort study was conducted in Guangdong, China, as a part of the National Free Pre-Pregnancy Checkups Project. PM2.5 exposure was estimated by using the inverse distance weighting method. To investigate the moderating effects of TSH levels on trimester-specific PM2.5 exposure and PTB, we used the Cox proportional hazards model. Additionally, to identify the susceptible exposure windows for weekly specific PM2.5 exposure and PTB, we built distributed lag models incorporating Cox proportional hazards models. Results: A total of 633,516 women who delivered between January 1, 2014, to December 31, 2019, were included. In total, 34,081 (5.4%) of them had abnormal preconception TSH levels. During the entire pregnancy, each 10-µg/m3 increase in PM2.5 was linked to elevated risks of PTB (hazard ratio [HR] 1.559, 95% CI 1.390-1.748), early PTB (HR 1.559, 95% CI 1.227-1.980), and late PTB (HR 1.571, 95% CI 1.379-1.791) among women with abnormal TSH levels. For women with normal preconception TSH levels, PM2.5 exposure during the entire pregnancy was positively associated with the risk of PTB (HR 1.345, 95% CI 1.307-1.385), early PTB (HR 1.203, 95% CI 1.126-1.285), and late PTB (HR 1.386, 95% CI 1.342-1432). The critical susceptible exposure windows were the 3rd-13th and 28th-35th gestational weeks for women with abnormal preconception TSH levels, compared to the 1st-13th and 21st-35th gestational weeks for those with normal preconception TSH levels. Conclusions: PM2.5 exposure was linked with a higher PTB risk, particularly in women with abnormal preconception TSH levels. PM2.5 exposure appears to have a greater effect on pregnant women who are in the early or late stages of pregnancy.

Effects of maternal exposure to biomass cooking fuel on birth size and body proportionality in full-term infants born by vaginal delivery.

It remains unclear whether and how maternal exposure to biomass fuel influences infant anthropometry or body proportionality at birth, which are linked to their survival, physical growth, and neurodevelopment. Therefore, this study seeks to explore the association between household-level exposure to biomass cooking fuels and infant size and body proportionality at birth among women in rural Bangladesh. A total of 909 women were derived from the Pregnancy Weight Gain study, which was conducted in Matlab, a rural area of Bangladesh. Infant's weight (g), length (cm), head circumference (cm), small for gestational age (SGAW), short for gestational age (SGAL), low head circumference for gestational age (SGAHC), ponderal index, and cephalization index at birth were the outcomes studied. Of the women, 721 (79.3%) were dependent on biomass fuel. Compared to infants born to mothers who used gas for cooking, those born to biomass users had lower weight (ß - 94.3, CI - 155.9, - 32.6), length (ß - 0.36, 95% CI - 0.68, - 0.04), head circumference (ß - 0.24, CI - 0.47, - 0.02) and higher cephalization index (ß 0.03, CI 0.01, 0.05) at birth. Maternal biomass exposure is more likely to lead to symmetric SGA, although there is evidence for some brain-sparing effects.

Associations of air pollution exposures in preconception and pregnancy with birth outcomes and infant neurocognitive development: analysis of the Complex Lipids in Mothers and Babies (CLIMB) prospective cohort in Chongqing, China.

OBJECTIVES: To investigate the associations of traffic-related air pollution exposures in early pregnancy with birth outcomes and infant neurocognitive development. DESIGN: Cohort study. SETTING: Eligible women attended six visits in the maternity clinics of two centres, the First Affiliated Hospital of Chongqing Medical University and Chongqing Health Centre for Women and Children. PARTICIPANTS: Women who were between 20 and 40 years of age and were at 11-14 weeks gestation with a singleton pregnancy were eligible for participation. Women were excluded if they had a history of premature delivery before 32 weeks of gestation, maternal milk allergy or aversion or severe lactose intolerance. 1273 pregnant women enrolled in 2015-2016 and 1174 live births were included in this analysis. EXPOSURES: Air pollution concentrations at their home addresses, including particulate matter with diameter ≤2.5 µm (PM2.5) and nitrogen dioxide (NO2), during pre-conception and each trimester period were estimated using land-use regression models. OUTCOME MEASURES: Birth outcomes (ie, birth weight, birth length, preterm birth, low birth weight, large for gestational age and small for gestational age (SGA) status) and neurodevelopment outcomes measured by the Chinese version of Bayley Scales of Infant Development. RESULTS: An association between SGA and per-IQR increases in NO2 was found in the first trimester (OR: 1.57, 95% CI: 1.06 to 2.32) and during the whole pregnancy (OR: 1.33, 99% CI: 1.01 to 1.75). Both PM2.5 and NO2 exposure in the 90 days prior to conception were associated with lower Psychomotor Development Index scores (ß: -6.15, 95% CI: -8.84 to -3.46; ß: -2.83, 95% CI: -4.27 to -1.39, respectively). Increased NO2 exposure was associated with an increased risk of psychomotor development delay during different trimesters of pregnancy. CONCLUSIONS: Increased exposures to NO2 during pregnancy were associated with increased risks of SGA and psychomotor development delay, while increased exposures to both PM2.5 and NO2 pre-conception were associated with adverse psychomotor development outcomes at 12 months of age. TRIAL REGISTRATION NUMBER: ChiCTR-IOR-16007700.

[Association between maternal peri-conceptional exposures and risk of hypospadias and cryptorchidism in offspring].

Objective: To investigate the relationship between maternal exposures to peri-conceptional risk factors and the risk of hypospadias and cryptorchidism in offspring. Methods: Pregnant women who delivered male newborns and participated in the China birth cohort study between February 2018 and December 2020 at the research center of Beijing Obstetrics and Gynecology Hospital, Capital Medical University were selected for the study. All were enrolled at 6-13+6 weeks of their gestation. Baseline risk factor information was collected by questionnaire survey. Information on the outcome of hypospadias and cryptorchidism was obtained by clinical examination at birth and ultrasonography. Logistic regression was used to analyze the Odds Ratio (OR) and 95% Confidence Interval (95%CI) of each factor with respect to the onset of the outcome. Results: A total of 15, 833 pregnant women with an average age of (31.81±3.84) years were included. Among their offsprings, 113 were diagnosed as hypospadias or cryptorchidism (42 hypospadias, 69 cryptorchidism, and 2 both hypospadias and crypterchidism), with an incidence of 7.14‰. The results of multivariate logistic regression analysis showed that mothers with pregnancy history of birth defects (OR=3.01, 95%CI: 1.09-8.35), with preconception Hepatitis B infection (OR=4.74, 95%CI: 1.10-20.42), fetal growth restriction (OR=4.02, 95%CI: 2.10-7.68), multivitamin use since preconception (OR=1.98, 95%CI: 1.12-3.52), and never cook and eat at home (OR=2.17, 95%CI: 1.23-3.82) were risk factors for hypospadias and cryptorchidism (all P<0.05). Conclusions: Obesity in early pregnancy, preconception Hepatitis B infection, pregnancy history of birth defects, fetal growth restriction, multivitamin use before pregnancy, and rarely cook and eat at home were associated with an increased risk of hypospadias or cryptorchidism in their offsprings.

Maternal bisphenols exposure and thyroid function in children: a systematic review and meta-analysis.

Background: Evidence from animal experiments and epidemiological studies has reported controversial results about the effects of prenatal bisphenols (BPs) exposure on childhood thyroid function. This study aims to explore the associations of prenatal exposure to BPs with thyroid-related hormones (THs) in newborns and early childhood, with a particular focus on the sex-dependent and exposure level effects. Methods: Correlated studies were systematically searched from PubMed, Web of Science, Medline, Cochrane, and Embase until February 21, 2024. The exposures assessed include bisphenol A (BPA), bisphenol F (BPF), bisphenol S (BPS), bisphenol AF (BPAF), and tetrachlorobisphenol A (TCBPA). THs measured were thyroid stimulating hormone (TSH), total tri-iodothyronine (TT3), total thyroxine (TT4), free tri-iothyronine (FT3), and free thyroxine (FT4). Effect estimates were quantified using coefficients from multivariable regression models. Statistical analyses were completed using Stata 16.0. The methodological quality of the included studies was evaluated using the Newcastle-Ottawa Scale (NOS). Results: Eleven cohort studies comprising 5,363 children were included in our meta-analysis. Prenatal bisphenol concentrations were statistically significant related to alterations in thyroid hormones in children, exclusively in female offspring, including reduced TSH (ß = -0.020, 95% CI: -0.036, -0.005) and increased TT3 levels (ß = 0.011, 95% CI: 0.001, 0.021), and exposure to high concentration of bisphenols (>1.5 ug/g creatinine) significantly reduced FT3 levels in children (ß = -0.011, 95% CI: -0.020, -0.003). Conclusion: Prenatal bisphenol exposure is linked to alterations in thyroid hormone levels in girls, necessitating enhanced measures to control bisphenol exposure levels during pregnancy for child health protection. Systematic Review Registration: https://inplasy.com, identifier INPLASY202450129.

Urinary polycyclic aromatic hydrocarbon (PAH) metabolite concentrations in three pregnancy cohorts from 7 U.S. study sites.

OBJECTIVE: Prenatal exposure to polycyclic aromatic hydrocarbons (PAHs) is associated with adverse birth and developmental outcomes in children. We aimed to describe prenatal PAH exposures in a large, multisite U.S. consortium. METHODS: We measured 12 mono-hydroxylated metabolites (OH-PAHs) of 7 PAHs (naphthalene, fluorene, phenanthrene, pyrene, benzo(c)phenanthrene, chrysene, benz(a)anthracene) in mid-pregnancy urine of 1,892 pregnant individuals from the ECHO PATHWAYS consortium cohorts: CANDLE (n = 988; Memphis), TIDES (n = 664; Minneapolis, Rochester, San Francisco, Seattle) and GAPPS (n = 240; Seattle and Yakima, WA). We described concentrations of 8 OH-PAHs of non-smoking participants (n = 1,695) by site, socioeconomic characteristics, and pregnancy stage (we report intraclass correlation coefficients (ICC) for n = 677 TIDES participants). RESULTS: Exposure to the selected PAHs was ubiquitous at all sites. 2-hydroxynaphthalene had the highest average concentrations at all sites. CANDLE had the highest average concentrations of most metabolites. Among non-smoking participants, we observed some patterns by income, education, and race but these were not consistent and varied by site and metabolite. ICCs of repeated OH-PAH measures from TIDES participants were ≤ 0.51. CONCLUSION: In this geographically-diverse descriptive analysis of U.S. pregnancies, we observed ubiquitous exposure to low molecular weight PAHs, highlighting the importance of better understanding PAH sources and their pediatric health outcomes attributed to early life PAH exposure.

[Research progress on the developmental toxicity and mechanism of brominated flame retardants during pregnancy exposure on offspring].

Brominated flame retardants (BFRs) are a kind of brominated compounds widely used in electronic and electrical appliances, textiles, construction materials and other industrial products to improve the flame retardant property. Because of its strong chemical stability, environmental persistence, long-distance transmission, biological accumulation, the exposure of humans and organisms in the ecosystem is increasing, and its potential biological effects are of great concern. Now BFRs can be detected in breast milk, serum, placenta and cord blood. Studies have shown that exposure to BFRs during pregnancy can lead to adverse birth outcomes such as low birth weight, malformation, gestational age changes and impairment of neurobehavioral development. This article summarizes the pollution and population exposure of three traditional BFRs, polybrominated diphenyl ethers (PBDEs), hexabromocyclododecane (HBCD), and tetrabromobisphenol A (TBBPA), as well as the impact and mechanism of prenatal exposure on offspring birth outcomes and growth and development. It explores the harm of prenatal exposure to BFRs to offspring and proposes preventive measures for occupational populations for reference.

Prenatal Exposure to Ambient Air Pollution and Cerebral Palsy.

Importance: Air pollution is associated with structural brain changes, disruption of neurogenesis, and neurodevelopmental disorders. The association between prenatal exposure to ambient air pollution and risk of cerebral palsy (CP), which is the most common motor disability in childhood, has not been thoroughly investigated. Objective: To evaluate the associations between prenatal residential exposure to ambient air pollution and risk of CP among children born at term gestation in a population cohort in Ontario, Canada. Design, Setting, and Participants: Population-based cohort study in Ontario, Canada using linked, province-wide health administrative databases. Participants were singleton full term births (≥37 gestational weeks) born in Ontario hospitals between April 1, 2002, and March 31, 2017. Data were analyzed from January to December 2022. Exposures: Weekly average concentrations of ambient fine particulate matter with a diameter 2.5 µm (PM2.5) or smaller, nitrogen dioxide (NO2), and ozone (O3) during pregnancy assigned by maternal residence reported at delivery from satellite-based estimates and ground-level monitoring data. Main outcome and measures: CP cases were ascertained by a single inpatient hospitalization diagnosis or at least 2 outpatient diagnoses for children from birth to age 18 years. Results: The present study included 1 587 935 mother-child pairs who reached term gestation, among whom 3170 (0.2%) children were diagnosed with CP. The study population had a mean (SD) maternal age of 30.1 (5.6) years and 811 745 infants (51.1%) were male. A per IQR increase (2.7 µg/m3) in prenatal ambient PM2.5 concentration was associated with a cumulative hazard ratio (CHR) of 1.12 (95% CI, 1.03-1.21) for CP. The CHR in male infants (1.14; 95% CI, 1.02-1.26) was higher compared with the CHR in female infants (1.08; 95% CI, 0.96-1.22). No specific window of susceptibility was found for prenatal PM2.5 exposure and CP in the study population. No associations or windows of susceptibility were found for prenatal NO2 or O3 exposure and CP risk. Conclusions and relevance: In this large cohort study of singleton full term births in Canada, prenatal ambient PM2.5 exposure was associated with an increased risk of CP in offspring. Further studies are needed to explore this association and its potential biological pathways, which could advance the identification of environmental risk factors of CP in early life.

Association of alkylphenols exposure with serum liver function markers in pregnant women in Guangxi, China.

The liver toxicity of alkylphenols (APs) has been demonstrated in animal studies. However, relevant epidemiological evidence is still lacking in humans, especially during pregnancy. We obtained the levels of biochemical indicators of liver function in early (<13 weeks, mean gestation=9.80±1.96 weeks) and late (≥32 weeks, mean gestation = 37.23±2.45 weeks) pregnancies from 219 pregnant women in the Guangxi Zhuang birth cohort from 2015-2017. We also examined the serum levels of APs in these pregnant women in early pregnancy. The present study aimed to investigate the correlations between the exposure of pregnant women to APs and their serum liver function indices. The results of the generalized linear model (GLM) in this study revealed that nonylphenol (NP) was positively correlated with total bilirubin (TBIL) (P=0.04) in early pregnancy, and 4-n-nonylphenol (4-N-NP) was negatively correlated with glutamyl transferase (GGT) (P=0.012). In late pregnancy, NP was positively associated with TBIL (P=0.002), and 4-tert-octylphenol (4-T-OP) was positively correlated with alanine aminotransferase (ALT) (P=0.02). Restricted cubic spline (RCS) results revealed doseresponse relationships between NP and TBIL (Poverall=0.011) and between 4-N-NP and GGT (Poverall=0.007) in early pregnancy. In late pregnancy, there were doseresponse relationships between NP and TBIL (Poverall=0.001) and between 4-T-OP and ALT (Poverall=0.033). There was also a doseresponse relationship between NP volume and GGT with an inverted 'U' shape (Poverall=0.041, Pnonlinear=0.012). Bayesian kernel machine regression modeling (BKMR) revealed that TBIL increased significantly (P<0.05) with increasing levels of coexposure to APs in both early and late pregnancy. Overall, exposure to APs during pregnancy affects maternal liver function to varying degrees. The present study provides new epidemiological evidence that exposure to alkylphenols in pregnant women interferes with liver function.

Maternal exposure to heat and its association with miscarriage in rural KwaZulu-Natal, South Africa: A population-based cohort study.

BACKGROUND: We sought to improve the current understanding of how climate change impacts women's reproductive health in sub-Saharan Africa. OBJECTIVES: We investigated the relationship between maternal heat exposure and miscarriage (pregnancy ending before 20 weeks gestation) in a South African setting. DESIGN: Population-based cohort study. METHODS: Our study involved data for pregnancies collected via a health and demographic surveillance system in rural KwaZulu-Natal, South Africa between 2012 and 2016. Data from the South African Weather Service were used to compute maternal exposure to heat during the following time windows for each pregnancy: during the month preceding conception (T1) and during the week preceding the study outcome (either a miscarriage or no miscarriage, T2). Heat exposure was operationalized as a continuous variable and defined as the number of days that a mother was exposed to a mean daily temperature of > 26.6°C (A "hot day," equivalent to a mean daily temperature of > 80°F) during T1 or T2. Binary logistic regression was used to investigate the relationship between maternal heat exposure and miscarriage. RESULTS: A total of 105/3477 pregnancies included in our analysis ended in miscarriage (3.0%). Each additional hot day during T1 was associated with a 26% higher odds of miscarriage (odds ratio: 1.26; 95% confidence interval: 1.15-1.38). No significant associations were observed between maternal heat exposure during T2 and the odds of miscarriage (odds ratio: 0.94, 95% confidence interval: 0.73-1.20). The relationship between maternal heat exposure during T1 and the odds of miscarriage was J-shaped. CONCLUSION: There is a clear relationship between maternal heat exposure during the month preceding conception and miscarriage in our sub-Saharan African setting. Given the lack of feasible strategies to reduce pregnancy loss associated with prevailing high temperatures in sub-Saharan Africa, progressive climate change will likely exacerbate existing challenges for women's reproductive health in this region.

Effects of whole life-cycle exposure to carbaryl on reproduction of female marine medaka (Oryzias melastigma) and their offspring.

Carbaryl is widely used as a highly effective insecticide which harms the marine environment. This study aimed to assess the reproductive toxicity of chronic carbaryl exposure on female marine medaka and their female offspring. After a 180-day exposure from embryonic period to adulthood, females exhibited reduced attraction to males, decreased ovulation, increased gonadosomatic index and a higher proportion of mature and atretic follicles. These reproductive toxic effects of carbaryl may stem from changes in hormone levels and transcription levels of key genes along the HPG axis. Furthermore, maternal carbaryl exposure had detrimental effects on the offspring. F1 females showed the reproductive disorders similar to those observed in F0 females. The significant changes in the transcription levels of DNA methyltransferase and demethylase genes in the F0 and F1 generations of ovaries indicate changes in their DNA methylation levels. The changes in DNA methylation levels in F1 female marine medaka may lead to changes in the expression of certain reproductive key genes, such as an increase in the transcription level of cyp19a, which may be the reason for F1 reproductive toxicity. These findings indicate that maternal exposure may induce severe generational toxicity through alterations in DNA methylation levels. This study assesses the negative impacts of whole life-cycle carbaryl exposure on the reproductive and developmental processes of female marine medaka and its female offspring, while offering data to support the evaluation of the ecological risk posed by carbaryl in marine ecosystems.

Microcystin-LR prenatal exposure induces coronary heart disease through macrophage polarization imbalance mediated by trophoblast-derived extracellular vesicles.

Microcystin-leucine arginine (MC-LR) has been reported to exhibit placental toxicity, leading to potential adverse pregnancy outcomes. Placental abnormalities often coincide with congenital heart defects (CHD). However, the extent to which MC-LR-induced placental abnormalities contribute to CHD and the cellular mechanisms underlying this association remain unknown. In this study, we observed abnormal polarization of placental macrophages in pregnant mice exposed to MC-LR during pregnancy, and the embryos developed cardiac developmental defects that persisted into adulthood. Trophoblast-derived extracellular vesicles (T-EVs) increase in number during pregnancy and act as a critical signal in macrophage polarization. However, MC-LR significantly affected the miRNA expression profile of T-EVs. Upon internalization into macrophages, T-EV-derived miR-377-3p specifically targets the 3'UTR region of NR6A1 to inhibit gene expression. Silencing of transcription suppressor NR6A1 leads to abnormal activation of the downstream mTOR/S6K1/SREBP pathway, inducing metabolic reprogramming and ultimately leading to M1 polarization of macrophages. This study elucidated the placental mechanism underlying MC-LR-induced CHD for the first time, providing insights into the environmental risks associated with CHD.

[Research progress on the association between prenatal exposure to air pollutants and hypospadias in the offspring].

Recent epidemiological studies have increasingly found that pregnant women who are exposed to air pollutants (for example airborne particulate matter, nitrogen oxides, ozone, and sulfur dioxide) increase the risk of various birth defects in their offspring, such as congenital heart disease, neural tube defects, cleft lip and palate, and hypospadias. Hypospadias not only impairs the sexual function of infants but also causes major social and psychological problems during their growth period, therefore, the prevention and treatment of hypospadias infant carry substantial public health importance. However, the association between prenatal exposure to air pollution and hypospadias remains controversial. The study reviews the epidemiological research progress and potential biological mechanisms of prenatal maternal exposure to air pollutants such as particulate matter, nitrogen oxides, ozone, sulfur dioxide, and the risk of hypospadias in offspring. The study also summarizes the limitations of previous research and looks forward to future research directions, to provide scientific evidence for creating a healthy living environment for pregnant women, and reducing the risk of hypospadias in offspring.