Effect of prenatal exposure to phthalates on birth weight of offspring: A meta-analysis.

Prenatal exposure to phthalates is common. However, its effect on birth weight has always been met with conflicting conclusions. To explore the effects of prenatal phthalate exposure on neonatal weight, we searched PubMed, Web of Science (WOS), Cochrane Library, and Embase databases for articles published up to October 24, 2023. Observational studies with 95% confidence intervals (CI) were included. Our findings indicate no significant association between either mixed exposure effects or single phthalate metabolites and offspring birth weight when monitoring maternal urine phthalate metabolites. When stratified by sex, ΣHMWPs and MMP significantly reduced the birth weight of female offspring (ΣHMWPs: Pooled ß = -62.08, 95%CI: -123.11 to -1.05, P = 0.046; MMP: Pooled ß = -10.77, 95%CI: -18.74 to -2.80, P = 0.008). The results of subgroup analysis showed that ΣPAEs and ΣDEHP significantly decreased birth weight in the specific gravity correction group (ΣPAEs: Pooled estimates = -29.31, 95%CI: -58.52 to -0.10, P = 0.049; ΣDEHP: Pooled estimates = -18.25, 95%CI: -33.03 to -3.47, P = 0.016), and MECPP showed a positive correlation in the creatinine correction group (MECPP: Pooled estimates = 18.45, 95%CI: 0.13 to 36.77, P = 0.048). MEP and MBzP were negatively associated with birth weight in the no adjustment for gestational age group (MEP: Pooled estimates = -7.70, 95%CI: -14.19 to -1.21, P = 0.020; MBzP: Pooled estimates = -9.55, 95%CI: -16.08 to -3.03, P = 0.004). To make the results more convincing, more high-quality studies with large samples are urgently required.

Associations between maternal exposure to perfluoroalkylated substances (PFASs) and infant birth weight: a meta-analysis.

The objective of this study was to determine the associations between maternal exposure to PFASs and infant birth weight and to explore evidence for a possible dose-response relationship. Four databases including PubMed, Embase, Web of Science, and Medline before 20 September 2022 were systematically searched. A fixed-effect model was used to estimate the change in infant birth weight (g) associated with PFAS concentrations increasing by 10-fold. Dose-response meta-analyses were also conducted when possible. The study follows the guidelines of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). A total of 21 studies were included. Among these studies, 18 studies examined the associations between PFOA and birth weight, 17 studies reported PFOS, and 11 studies discussed PFHxS. Associations between PFHxS (ES = -5.67, 95% CI: -33.92 to 22.59, P = 0.694) were weaker than those for PFOA and PFOS (ES = -58.62, 95% CI: -85.23 to -32.01, P < 0.001 for PFOA; ES = -54.75, 95% CI: -84.48 to -25.02, P < 0.001 for PFOS). The association was significantly stronger in the high median PFOS concentration group (ES = -107.23, 95% CI: -171.07 to -43.39, P < 0.001) than the lower one (ES = -29.15, 95% CI: -63.60 to -5.30, P = 0.097; meta-regression, P = 0.045). Limited evidence of a dose-response relationship was found. This study showed negative associations between maternal exposure to PFASs and infant birth weight. Limited evidence of a dose-response relationship between exposure to PFOS and infant birth weight was found. Further studies are needed to find more evidence.

Maternal exposure to pesticides and autism or attention-deficit/hyperactivity disorders in offspring: A meta-analysis.

OBJECTIVE: To analyze the association between maternal pesticide exposure and autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorders (ADHD) in offspring. METHOD: Five databases including PubMed, Embase, Web of Science, Medline, as well as PsycINFO were systematically retrieved for the records related to pesticide exposure during pregnancy and ASD and ADHD in offspring before August 30, 2022. The pesticide category, maternal age and window of exposure as the main subgroups were presented. RESULTS: 949 studies were initially identified, and 19 studies were eventually included. Eleven were on ASD, seven were on ADHD, and one was on both disorders. Maternal pesticide exposure was positively related to ASD (pooled OR = 1.19 (95%CI: 1.04 to 1.36)) and ADHD (pooled OR = 1.20 (95%CI: 1.04 to 1.38)) in offspring. In the subgroup analysis, organophosphorus pesticides (OPs) (pooled OR = 1.14 (95%CI: 1.04 to 1.24)), pyrethroid (pooled OR = 1.40 (95%CI: 1.09 to 1.80)), and maternal age ≥30 years old (pooled OR = 1.24 (95%CI: 1.10 to 1.40)) increased the risk of ASD in offspring. Maternal organochlorine pesticides (OCPs) exposure was a risk factor for ADHD in offspring (pooled OR = 1.22 (95%CI: 1.03 to 1.45)). CONCLUSION: Maternal pesticide exposure increased the risk of ASD and ADHD in offspring. Moreover, OPs, pyrethroid, and maternal age ≥30 years old were found to be risk factors affecting children's ASD. Maternal exposure to OCPs increased the risk of ADHD in offspring. Our findings contribute to our understanding of health risks related to maternal pesticide exposure and indicate that the in utero developmental period is a vulnerable window-of-susceptibility for ASD and ADHD risk in offspring. These findings should guide policies that limit maternal exposure to pesticides, especially for pregnant women living in agricultural areas.