Table 1.
Growth and neurodevelopment effects from exposure to electronic waste
| Exposure setting | Exposed population | Control population | Toxic chemicals | Health outcomes | |
|---|---|---|---|---|---|
| Growth | |||||
| Huo et al (2019)60 | Cross-sectional: exposed area vs reference area, China | 155 pregnant women (mean age 26·63 years) | 102 pregnant women (mean age 27·68 years) | PAHs | Urinary ∑OHPAH=6·87 mg/g cre exposed vs 3·90 mg/g cre control (p<0·001); dominant metabolites=2-OHNap and 1-OHPyr. Elevated ∑OHPAHs associated with a decrease of 235 g in bodyweight (95% CI −452 to −17), decrease of 1·72 cm in head circumference (−2·96 to −0·48), decrease of 1·06 kg/m2 in BMI (−1·82 to −0·31), and decrease of 0·42 in Apgar1 score (−0·66 to −0·18; all p<0·05). |
| Li et al (2018)65 | Cross-sectional: exposed town vs reference town, China | 150 pregnant women (mean age 26·51 years) | 150 pregnant women (mean age 28·43 years) | PBDEs | ∑14PBDEs in umbilical cord=71·92 ng/g lw vs 15·52 ng/g lw (p<0·001) and negatively correlated with neonatal BMI (r=−0·20), Apgar1 score (r=−0·39), and head circumference (r=−0·37; all p<0·01). |
| Xu et al (2016)20 | Cross-sectional: exposed town vs reference town, China | 99 pregnant women (mean age 25·05 years) | 86 pregnant women (mean age 27·96 years) | Lead and cadmium | Placental lead=498 ng/g wt vs 27 ng/g wt (p<0·01); cadmium=96·19 ng/g wt vs 12·65 ng/g wt (p<0·01). Shorter neonatal length in exposed =49·78 vs 50·30 cm (p<0·01). Cadmium negatively correlated with neonatal weight (B=−0·20) and length (B–0·44; both p<0·05). Lead was not statistically associated with birth outcomes (p>0·05). 32 differentially expressed proteins identified from 54 protein spots, FUM expression lower in exposed placenta (605 pg/g wt vs 1019 pg/g wt; p<0·05). |
| Xu et al (2015)66 | Cross-sectional: exposed group vs reference group, China | 69 pregnant women (mean age 26·4 years) | 86 pregnant women (mean age 27·8 years) | PBDEs | Placental ∑PBDE=32·25 ng/g lw vs 5·13 ng/g lw; common congener=BDE −209, −28, −153, −183, −47, −99. Neonatal BMI=11·90 kg/m2vs 12·69 kg/m2, Apgar1 score=9·16 vs 10·0, and head circumference=33·52 cm vs 34·92 cm (all p<0·001). PBDE and BDE-47 negatively correlated with BMI, head circumference, and Apgar1 score, negative correlation between BDE-99 and BMI, BDE-28/153 and Apgar 1 score, and BDE-183 and BMI and Apgar1 score (all p<0·05). |
| Zhang et al (2018)56 | Cross sectional: exposed town vs reference town, China | 237 mother–neonate pairs (mean maternal age 26·29 years) | 212 mother–neonate pairs (mean maternal age 28·52 years) | Cadmium | Maternal urinary cadmium with male neonates=1·38 μg/g cre vs 0·75 μg/g cre, urinary cadmium with female neonates=1·59 μg/g cre vs 0·76 μg/g cre (both p<0·001). Urinary cadmium negatively associated with birthweight (β=−0·16), length (β=−0·17), head circumference (β=−0·38), Apgar1 and Apgar5 score (β=−0·26 and β=−0·43) in female neonates (all p<0·05), in male neonates urinary cadmium negatively associated with Apgar1 score (β=−0·21; p<0·01). |
| Xu et al (2015)21 | Cross-sectional: exposed town vs reference town, China | 95 children aged 3–7 years | 72 children aged 3–7 years | PAHs and lead | ∑16PAHs in blood=68·53 μg/L vs 26·92 μg/L, ∑7 carcinogenic PAHs=60·27 μg/L vs 21·30 μg/L, blood lead 13·89 μg/dL vs 8·55 μg/dL (all p<0·01). Blood lead negatively correlated with child height (Rs=−0·16; p<0·05); child height (β=−3·88) and chest circumference (β=−1·15) negatively associated with ∑16PAHs (p<0·05). |
| Yang et al (2013)22 | Cross-sectional: e-waste processing area, China | 246 kindergarten children aged 3–8 years | None | Lead and cadmium | Blood lead=7·30 μg/dL, blood cadmium=0·69 μg/L. Blood lead negatively associated with height (β=−0·10), weight (β=−0·14; both p<0·05), and positively associated with increase urinary excretion of DPD (mean 10·09 [SD 3·76 nmol/g]; p<0·01). No association between cadmium and bone, calcium metabolic biomarker (p>0·05). |
| Zeng et al (2019)23 | Cross sectional: exposed town vs reference town, China | 300 preschool children (mean age 4·66 years) | 170 preschool children (mean age 4·34 years) | Lead, cadmium, chromium, and manganese | Blood lead=6·81 μg/dL vs 4·98 μg/dL, blood cadmium=0·66 μg/L vs 0·54 μg/L, PM2·5=57·73 μg/m3vs 40·53 μg/m3, elevated lead and cadmium in PM2·5 (data not shown; all p<0·05). Lower birth length, weight, BMI in exposed (all p<0·05), blood lead negatively associated with height (β=−0·06), weight (β=−0·12), head circumference (β=−0·12), and chest circumference (β=−0·10; all p<0·05). No association between cadmium, chromium, manganese with growth parameters (p>0·05). |
| Neurodevelopment | |||||
| Cai et al (2019)24 | Cross-sectional: exposed town vs control town, China | 358 preschool children (aged 3–6 years) | 216 preschool children (aged 3–6 years) | Lead | Blood lead=4·88 μg/dL vs 3·47 μg/dL (p<0·001), serum cortisol=452 ng/mL vs 593 ng/mL (p<0·001), cortisol negatively associated with blood lead (B=−0·13, 95% CI −0·27 to −0·003; p<0·05). Elevated blood lead (>5 μg/dL) increased sensory integration difficulty scores (hearing, touch, body awareness, balance and motion, total sensory systems, r=0·10–0·18; p<0·05), scale for touch negatively correlated with serum cortisol levels (r=−0·16; p<0·05). |
| Liu et al (2015)25 | Cross-sectional: exposed town vs control town, China | 135 children (mean age 38 months) | 149 children (mean age 39 months) | Lead | Blood lead=11·30 μg/dL vs 5·77 μg/dL, lower cognitive scores (100 vs 120) and language scores (100 vs 111; both p<0·001), no differences of DRD2 genotypes among exposed (p>0·05). Blood lead related to reduced cognitive (β=−0·19) and language scores (β=−0·72; both p<0·001). No association between DRD2 polymorphism and cognitive or language scores (p>0·05). |
| Liu et al (2014)26 | Cross-sectional: e-waste disposal site, China | 240 kindergarten children aged 3–7 years | None | Lead, cadmium, and manganese | Blood lead=7·33 μg/dL, blood cadmium=0·69 μg/L, blood manganese=17·98 μg/L, serum S100β=0·12 μg/L. ADHD prevalence=18·6% (higher prevalence in males than in females). Blood lead, cadmium, and manganese correlated with conduct problems and antisocial behaviour (data not shown), serum S100β positively correlated with blood lead (≥10 μg/dL, r=0·47) and some behavioural abnormalities (p<0·05). |
| Zhang et al (2015)27 | Cross-sectional: e-waste recycling town, China | 243 preschool children (aged 3–7 years) | None | Lead and cadmium | Blood lead=7·9 μg/dL, blood cadmium=0·95 μg/L, ADHD=12·8%. Positive correlations between blood lead and ADHD scores (inattentive, hyperactive/impulsive, and total scores, β=0·22–0·28; p<0·001). No correlation with blood cadmium. Elevated blood lead increased risk of ADHD (odds ratio 2·4, 95% CI 1·1 to 5·2). |
| Liu et al (2018)28 | Cross-sectional: exposed group vs reference group, China | 120 children (mean age 37·49 months) | 138 children (mean age 38·80 months) | Lead and cadmium | Blood lead=11·30 μg/dL vs 5·77 μg/dL, blood cadmium=1·22 μg/L vs 0·72 μg/L (both p<0·001). Lower cognitive (100 vs 120) and language scores (99 vs 111), higher TSH, and higher FT4 (all p<0·01). Blood lead negatively correlated with cognitive scores (β=−1·57) and language scores (β=−0·80; both p<0·001) in mediation analysis, no correlation between blood cadmium and language or cognitive scores (p>0·05). FT3, FT4, and TSH did not mediate between lead and mental development. |
PAH=polycyclic aromatic hydrocarbons. cre=creatinine. ∑OHPAH=total hydroxylated PAH. 2-OHNap=2-OHnaphthalene. 1-OHPyr=1-hydroxypyrene. BMI=body-mass index. Apgar1=Apgar score at 1 min. Apgar1=Apgar score at 5 mins. PBDE=polybrominated diphenyl ether. lw=lipid weight. wt=weight. FUM=fumarate hydratase. DPD=deoxypyridinoline. S100β=S100 calcium-binding protein β. DRD2=dopamine receptor-2. ADHD=attention-deficit hyperactivity disorder. TSH=thyroid stimulating hormone. FT4=free thyroxine. FT3=free triiodothyronine.