Organophosphate flame retardants (OPFRs) are increasingly and widely used as substitutes for brominated flame retardants in daily life. The chemical structure of OPFRs is very similar to that of organophosphorus pesticides, leading to concerns about their neurotoxicity. A few epidemiological studies have been published with inconsistent results on this topic, and a systematic scoping review is needed to provide an overview or map of the current evidence on the relationship of OPFRs with neurodevelopmental toxicity. Therefore, MEDLINE (accessed through PubMed), Web of Science, and CNKI (Chinese National Knowledge Infrastructure) were systematically searched for articles published in the last two decades. Nine eligible articles were included in the present systematic scoping review for adherence to the predefined PECOS (population, exposure, comparison, outcome, study design) statement. Six studies were conducted in the USA, and the remaining three studies were conducted in Austria, Norway and China. A total of 2 581 children (1 203 females and 1 378 males) were included. Half of the included studies focused on the adverse effects of OPFR exposure on cognition in children, while others primarily focused on the behaviors of children. In summary, the current evidence suggests inverse associations between early-life exposure to OPFRs and the childhood intelligence quotient and internalizing behavior and positive relationships of OPFR exposure with externalizing behavior. However, some differences in the timing of sample collection for exposure measurements, in the individual OPFR metabolites available, in the neurodevelopmental scales for outcome measurement, and in the statistical methods used to analyze the data are noted. In addition, further studies are warranted to evaluate some important issues, such as sex differences in the association, exposure-sensitive periods, and cumulative exposure risk assessment.

Thallium, a highly toxic heavy metal and priority pollutant, has been widely reported to cause neurodevelopmental toxicity in animals. However, accessible epidemiological studies concerning the neurodevelopmental toxicity of early-life thallium exposure in humans are limited. In a prospective birth cohort including 2164 mother-child pairs, we explored the effect of prenatal serum thallium exposure on cognitive development among preschool-aged children born in Ma'anshan, Anhui, China. Serum thallium concentrations were measured in the first trimester, second trimester, third trimester, and cord blood by inductively coupled plasma mass spectrometry (ICP-MS). Child cognitive development was appraised by the Chinese version of the Wechsler Preschool and Primary Scale of Intelligence-Fourth Edition (WPPSI-IV) at 4.5 years old. Multiple informants generalized estimating equations (GEEs) were fit to jointly estimate the association between the four repeated measurements of thallium concentrations and the preschool-aged children's cognitive test scores. After adjusting for potential confounders, the visual spatial index (VSI) was 1.45 points lower in the highest tertile of serum thallium during the first trimester than in the lowest tertile (p for trend = 0.04). Moreover, children in the highest tertile of serum thallium during the third trimester had a significantly lower full-scale intelligence quotient (FSIQ) (β = -1.51, 95% CI: -2.68, -0.35), VSI (β = -1.79, 95% CI: -3.16, -0.42), fluid reasoning index (FRI) (β = -1.41, 95% CI: -2.73, -0.10), and processing speed index (PSI) (β = -1.47, 95% CI: -2.71, -0.24) scores than the children in the lowest tertile. When performing stratified analysis by child sex, the associations of first- and third-trimester thallium concentrations with cognitive test scores were more prominent in boys than in girls. Our findings revealed that maternal serum thallium exposure during the first and third trimesters, but not other periods, had detrimental effects on preschoolers' cognitive development, and these effects showed sex differences.

Growth and development are a plastic process. ¹ The theory of developmental origins of health and disease, a hypothesis on the disease aetiology, has attracted worldwide interest since it appeared. Accumulating epidemiological evidence suggests that a sub-optimal intrauterine environment may affect pregnancy outcomes and the growth and development of offspring in later life. ² Researches have revealed that exposure to a variety of environmental chemicals in early life was closely associated with adverse birth outcomes, such as low birth weight (LBW), growth retardation and birth defects as well as children’s neurodevelopment. ^{3, 4} Environmental endocrine disruptors (EEDs), antibiotics and microplastics are among the international emerging contaminants. Phthalic acid esters (PAEs), bisphenols, polychlorinated biphenyl and some heavy metals are all included in EEDs. In recent years, the detrimental influence of maternal exposure to EEDs during infant growth and development has received increasing attention. Nevertheless, most of the existing studies have sampled EEDs at a single timepoint and have not systematically monitored exposures throughout pregnancy. There is also a lack of assessment of the sex-specific effects of maternal EEDs exposure on children’s development.