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Background The prevalence of allergic diseases in children has increased globally. Early-life exposure to inorganic arsenic has been found to be associated with impaired immune function and decreased lung function in children; however, the results are inconsistent. We aimed to evaluate the effect of prenatal and childhood exposure to inorganic arsenic on allergic diseases in children, through a 15-year follow-up birth cohort study, conducted in central Taiwan. Methods Children born to women enrolled in the Taiwan Maternal and Infant Cohort Study (TMICS-pilot) from December 2000 to November 2001 were recruited and followed every 2–3 years until the age of 14 years. Urinary specimens were collected in the pregnant women during the 3rd trimester and the followed children. Diagnoses of allergic diseases were based on physician diagnoses using the International Study of Asthma and Allergies in Childhood questionnaire. Urinary arsenic speciation was performed using high-performance liquid chromatography and inductively coupled plasma dynamic reaction cell mass spectrophotometry. Results Of the 261 children from 358 mother-infant pairs for this study, those with asthma and allergic rhinitis reported a higher prevalence of maternal allergy (49.47%) than did non-allergic children (29.81%). In the fully adjusted model, levels of maternal urine (iAs + MMA + DMA) greater than the median were found to be significantly associated with an increased risk of asthma (OR = 4.28; 95% CI 1.32, 13.85). Levels of urinary (iAs + MMA + DMA) in children higher than the median were associated with an increased risk of allergic rhinitis (OR = 2.26; 95% CI 1.20, 4.26). Conclusion Prenatal and childhood exposure to inorganic arsenic were found to be significantly associated with the occurrence of asthma and allergic rhinitis in children, respectively. Further large cohort follow-up studies are important to validate the association between inorganic arsenic exposure and allergic diseases in children.

Background: Inorganic arsenic (iAs) exposure potentially causes diabetes and cardiovascular diseases in adults. However, its effect on glucose and lipid metabolism in early life remains unknown. Objective: We evaluated the associations between early-life arsenic exposure and profiles of glucose and lipids in a 15-year birth cohort in central Taiwan. Methods: We studied 237 adolescents through 5 waves of follow-up interviews and examinations at ages of approximately 2, 5, 8, 11, and 14 y. We obtained at least one follow-up urine measurement for arsenic species and blood sample collection up to 14 y of age and identified group-based trajectories of serial iAs by semiparametric mixture modeling. Multiple linear and logistic regressions were performed to assess the effect of the arsenic exposure trajectory on serum fasting glucose, total cholesterol (TCHO), triglycerides (TGs), low-density lipoprotein cholesterol (LDL), and high-density lipoprotein cholesterol (HDL). Results: Three trajectories of postnatal arsenic exposure were identified, namely stable-low (31.4%), stable-high (48.2%), and rising-high (20.4%) groups. Compared with the stable-low trajectory group, the percent changes in TCHO and LDL was 14% (95% confidence interval 4–24%) and 23% (9–38%) for the group with “rising-high” trajectory and was 8% (−1–16%) and 16% (4–29%) for the group with “stable-high” trajectory. The rising-high group was also associated with an increase in the TCHO/HDL ratio by 14% (95% CI 3%–25%). The adjusted odds ratios of high developmental trajectories of TCHO, TG, LDL, and non-HDL levels were 4.0 (95% CI 1.2–13.7), 12.2 (2.2–67), 7.3 (1.8–30), and 3.6 (0.9–14.6), respectively, in the rising-high group (reference: stable-low group). Conclusion: Our findings suggest that conversion to an atherogenic lipid profile in adolescents may be associated with early-life exposure to environmental arsenic, particularly during the pre-adolescent period. An environmental modification approach for preventing As-related cardiovascular disease is recommended to begin early in life. Keywords: Arsenic, Lipid profile, Birth cohort, Trajectory, Glucose metabolism, Insulin resistance

Phthalic acid esters (PAE) are widely used during chemical synthesis and do not form covalent linkages with products. It has been reported that exposure to PAE affects the immune response. However, their effect on antibody concentrations in children is still under investigation. We aimed to examine the association between early-life phthalate exposure and antibody concentrations in children in a longitudinal birth cohort established in 2000–2001. We recruited 398 neonates in central Taiwan and followed them up every 2–3 years, with various antibody-related studies at 11- and 14-year follow-ups. Seven urinary phthalate metabolites were quantified in mothers during pregnancy and children aged 11 years. Four antibody concentrations were analyzed in children aged 11 and 14 years. The percent change in antibody concentrations from ages 11 to 14 years was calculated and its association with phthalate exposure was evaluated via multivariate regression analysis. Eighty-one followed-up children were with sufficient data. After adjusting for prenatal exposure and other confounders, double concentrations of the urinary sum of di-2-ethylhexyl phthalate (ΣDEHPm) and mono-n-butyl phthalate (MnBP) were associated with a 18.06% (95% CI = 3.34%, 32.78%) and 22.53% decrease (95% CI = 3.39%, 41.66%) in antibody concentration against hepatitis B, respectively. Phthalate exposure was found to be related to decreased antibody concentrations against hepatitis B (DEHP, DBnP) in the early teens. This exposure is suggested to be considered for clinical re-booster vaccines among junior high school students. Further verification with additional cohorts and studies on the underlying mechanisms of phthalate exposure are warranted.

Background: Lead (Pb) exposure is associated with children's neurodevelopment, even at low doses. Leaded gasoline was banned in Taiwan in 2000 to reduce environmental exposure to Pb. Objectives: To evaluate the neurodevelopmental effect of low-level Pb exposure in young children. Methods: In 2001–2002, we have recruited 430 pregnant women in the third-trimester in Taichung, Taiwan who answered detailed questionnaires in the obstetric clinic. A total of 119, 76, and 66 children were followed up at 2–3, 5–6 and 8–9 years, respectively. We collected blood samples from pregnant women, Umbilical cord and children, and evaluated children's neurodevelopment and cognition function at all three time points using Bayley and Wechsler tests. Blood samples were analyzed for whole blood lead (BPb) levels. Results: Geometric mean of BPb in pregnant women, cord blood and children at 2–3, 5–6 and 8–9 years old were 2.21, 1.30, 2.48, 2.49 and 1.97 μg/dl, respectively. Low-level postnatal Ln BPb was significantly associated with not only decreasing intelligence quotient (IQ), but also delayed cognitive function in children at 5–8 years (β: −5.97, SE: 2.59, p=0.025), after adjustment for maternal education, maternal BPb exposure, Home Observation for Measurement of the Environment Inventory (HOME), and gender of child, using linear mixed models. No significant relation was observed between prenatal and cord blood Pb levels and children's cognitive function in children 2–8 years. Conclusions: Low-level postnatal BPb levels in children at 2–5 years may have lagged effects on neurodevelopment in those at 5 to 8 years. Action is warranted to reduce even very low environmental Pb levels to reduce the developmental burden of Pb on children. Keywords: Children health, Blood lead, Intelligence quotient (IQ), Prenatal exposure, Postnatal exposure, Gasoline

We have previously reported on the effects of in utero exposure to polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) and polychlorinated biphenyls (PCBs) on thyroid function and growth hormone concentrations at birth and in two and five year-old children. Herein, we present our most recent follow-up examination findings for the same cohort of children at eight-years of age. A total of 56 children (23 boys, 33 girls) were examined. Bone age (BA), hormone concentrations, and indicators of reproductive development including Tanner, breast, genital, and armpit stages were assessed. Estradiol concentrations were significantly lower in children exposed to higher levels than median of PCDD/Fs+PCBs TEQ compared to the children exposed to levels lesser than median (P=0.003). Girls exposed to higher levels than median of indicator PCBs had a significantly greater proportion in genital stage 1 and shorter fundi and uteri lengths, as compared to those exposed to low levels (P=0.025 and P