Early life secondhand smoke exposure assessed by hair nicotine biomarker may reduce children's neurodevelopment at 2 years of age

Abstract

Exposure to secondhand smoke (SHS) can affect fetal brain development as well as subsequent neurodevelopment. This study aimed to determine the association between prenatal and postnatal SHS exposure with children's neurodevelopment at 2years of age. Among 107 mother-child pairs from a Malaysia prospective cohort, prenatal and postnatal SHS exposure was determined based on maternal and child hair nicotine concentrations. Multiple linear regressions were used to determine the association between prenatal and postnatal levels of nicotine in maternal and children's' hair with children's neurodevelopment. After adjustment for confounders, prenatal nicotine concentration levels were negatively associated with communication (β=-2.059; p=0.015) and fine motor skills (β=-2.120; p=0.002) while postnatal nicotine concentration levels were inversely associated with fine motors (β=-0.124; p=0.004) and problem solving skills (β=-0.117; p=0.013). In conclusion, this study suggests that early life exposure to SHS may affect children's neurodevelopment.

Systematic review showed that low and moderate prenatal alcohol and nicotine exposure affected early child development

“…Furthermore, neurodevelopment was only assessed by using a questionnaire that may lack adequate psychometric properties. This may have reduced the evidence of the presented results 39 …”

“…The effects on 24‐month‐old toddlers revealed that second‐hand smoke exposure during pregnancy was associated with lower neurodevelopment 39 . Affected children showed poorer fine motor skills, for example hand and finger movements, and impaired communication skills in vocalising, listening and understanding.…”

“…Deficits include lowered sensory regulatory responses 27 or lower communication and fine motor skills. 39 Thus, there is evidence that low and moderate consumption during pregnancy may also impair early child development in a complex way. Consumption of low to moderate amounts during pregnancy is more commonly practiced and more accepted than high-level intake in different societies and regions across the world.…”

Placental programming, perinatal inflammation, and neurodevelopment impairment among those born extremely preterm

“…The presence of multiple methylated CpG sites in CpG islands of promoters often causes stable silencing of genes, 71 although this gene silencing can also be initiated by other mechanisms. 71 The placental also serves as a sensor and transducer of environmental signals, such as prenatal exposure to tobacco, [72][73][74][75] air pollution, [76][77][78][79][80][81][82][83][84][85][86][87][88][89][90] and environmental pollutants, [91][92][93][94] which have been tied to both neonatal morbidities and perinatal inflammation. Important questions remain in relation to the role of specific biological pathways in the placenta that when perturbed can lead to child health or disease.…”

“…The placental also serves as a sensor and transducer of environmental signals, such as prenatal exposure to tobacco, 72 – 75 air pollution, 76 – 90 and environmental pollutants, 91 – 94 which have been tied to both neonatal morbidities and perinatal inflammation. Important questions remain in relation to the role of specific biological pathways in the placenta that when perturbed can lead to child health or disease.…”