Table 3.
Genetic and oxidative changes resulting from exposure to electronic waste
| Exposure setting | Exposed population | Control population | Toxic chemicals | Health outcomes | |
|---|---|---|---|---|---|
| Genetic | |||||
| 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 | Umbilical cord ∑14PBDEs=71·92 ng/g lw vs 15·52 ng/g lw (p<0·001). Lower expression of CAT=902 pg/g wt vs 1305 pg/g wt, GSTO1=526 pg/g wt vs 562 pg/g wt, Cyt c=389 pg/g wt vs 268 pg/g wt (all p<0·01). ∑14PBDEs, BDE-17, BDE-99, BDE-183 associated with decreased CAT expression (β=−0·31 to −0·10), GSTO1 decrease with BDE-153, BDE-190 (β=−0·20 to −0·16), BDE-99, BDE-190 increased Cyt c expression (β=0·16 to 0·19; all p<0·05). |
| Lin et al (2013)57 | Cross-sectional: exposed town vs non-polluted town, China | 227 healthy puerperae (mean age 26·45 years) | 93 healthy puerperae (mean age 27·63 years) | Lead and cadmium | Placental cadmium=0·09 μg/g vs 0·02 μg/g (p<0·01), lead=1·25 μg/g vs 1·35 μg/g (p>0·05). Placental telomere length negatively correlated with cadmium (r=−0·14; p<0·05), no correlation between placental lead and telomere length (r=0·03; p>0·05). Positive correlation between mean TRF length and T/S ratio (R2=0·79; p<0·01). residence during pregnancy in exposed associated with telomere length (OR=2·0, 95% CI 0·07 to 0·60). |
| Zeng et al (2019)36 | Cross sectional: exposed town vs reference town, China | 101 pregnant women (mean age 27·3 years) | 103 pregnant women (mean age 28·0 years) | Lead, cadmium, manganese, and chromium | Umbilical cord blood lead=7·34 μg/dL vs 3·07 μg/dL (p<0·001), no difference of umbilical cord blood cadmium, manganese, and chromium among groups (p>0·05). Methylation of BAI1 (cg25614253; 8% vs 7%, hyper-regulated), CTNNA2 (cg20208879; 62% vs 64%, hypo-regulated; all p<0·05), both correlated with umbilical cord blood lead (r=0·16 and r=−0·19; p<0·05). In adjusted regression, umbilical cord blood lead negatively associated with CTNNA2 (β=−1·20, 95% CI −2·13 to −0·26). No correlation between umbilical cord blood cadmium, manganese, chromium levels, and the methylation levels of two CpGs. |
| Huo et al (2014)34 | Cross sectional: exposed town vs reference town, China | 189 neonates and 319 children | 84 neonatesand 185 children | Lead | Blood lead in neonates (2004–05: 10·50 μg/dL vs 7·79 μg/dL; 2006: 9·41 μg/dL vs 5·49 μg/dL), children (2004–05: 15·31 μg/dL vs 9·94 μg/dL; 2006: 13·17 μg/dL vs 10·04 μg/dL; all p<0·05). No difference of ALAD genotypes between groups (p>0·05), no significant differences between blood lead and ALAD-1/ALAD-1 or ALAD-1/ALAD-2 among newborns and children (all p>0·05). |
| Xu et al (2020)37 | Cross-sectional: exposed town vs reference town, China | 68 preschool children aged 3–7 years | 48 preschool children aged 3–7 years | Lead and cadmium | Blood lead=5·29 μg/dL vs 3·63 μg/dL (p<0·001), urinary cadmium 1·52 μg/g vs 1·21 μg/g cre (p>0·05). Higher promoter methylation levels at cg02978827, position +14, and lower methylation at position +4 of Rb1 (all p<0·05), no difference of methylation in CASP8, MeCP2 among groups. Strong positive trend of MeCP2 promoter methylation with increasing lead (R2=0·709) and cadmium (R2=0·687), minimal negative trend of Rb1 (R2=0·014 and R2=0·015) and CASP8 (R2=0·001 and R2=0·002). |
| Li et al (2014)35 | Cross-sectional: close proximity (≤5 km to e-waste recycling) vs remote group (<40 km), China | 30 adult residents (mean age 41 years) | 28 adult residents (mean age 33 years) | Calcium, copper, iron, lead, zinc, selenium, magnesium, and POPs | Lead=90·39 μg/L vs 68·40 μg/L, copper=17·34 μM vs 15·20 μM, MDA=1·29 vs 0·25 nmol/mL, PCBs=42·59 vs 10·14, PBDEs=23·05 vs 14·60, calcium=1·71 nM vs 1·82 nM, zinc=101 μM vs 127 μM (all p<0·05). Micronucleus=18·27% vs 7·32% (p<0·001). CD4+/CD8+ T cell ratios, CD4+CD25nt/hiCD127lo regulatory T cell percentage, and CD95 expression higher in close proximity group (p>0·05). RNA expression genes: men detrimentally affected (p<0·05). |
| Yuan et al (2018)75 | Cohort study: exposed town (e-waste disposal center) vs control town, China | 3349 local residents | 2606 local residents | PCBs, PBDEs, and lipid-standardised serum POP | Increased PCBs, PBDEs, ageing signal pathway (P53, Rb, P16INK4a, and P14ARF in plasma), IL-6 and IL-10 (p<0·05, data not shown), increased TNF-α (p>0·05, data not shown) among exposed. Micronucleus=20·62% vs 7·21% (p<0·01), telomere loss=1·24% vs 0·10%, fragile telomere=2·76% vs 0·69%, decreased LINE-1 DNA methylation in exposed. PBDE-184 correlated with telomere shortening (r=−0·27; p<0·05). POP exposures associated with type 2 diabetes, autoimmune disorders, abnormal pregnancy, and foetal growth. |
| Li et al (2020)59 | Experiment site (e-waste residents and former workers) vs reference site, China | 23 local residents and 23 former workers, aged 30–50 years | 45 residents aged 30–50 years | 25 metals | Arsenic=17·24 ng/mL vs 15·42 ng/mL vs 10·84 ng/mL, nickel=4·01 ng/mL vs 4·76 ng/mL vs 1·95 ng/mL, silver=0·16 ng/mL vs 0·22 ng/mL vs 0·03 ng/mL, lanthanum=0·30 ng/mL vs 0·47 ng/mL vs 0·03 ng/mL, cerium=2·43 ng/mL vs 4·08 ng/mL vs 0·06 ng/mL (all p<0·05 between controls vs e-waste residents and controls vs former workers). Blood cerium negatively correlated with global DNA methylation among former workers (r=−0·51; p<0·05). |
| He et al (2015)78 | Cross sectional: exposed town vs non-exposed town, China | 23 adult residents (mean age 35 years) | 25 adult residents (mean age 35 years) | PCBs, BDE, DP, HCB, HCH, and DDE | PCBs=149 ng/g lipid vs 35 ng/g lipid, DPs=8·14 ng/g lipid vs 1·96 ng/g lipid, BDE congeners=16·33 ng/g lipid vs 14·28 ng/g lipid (all p<0·05). Higher ROS activity (data not shown) and micronucleus rate (16·74% vs 7·8%) in exposed (both p<0·05), no correlation between POPs (PBDE/DP/PCB) and micronucleus rate (p<0·05). Expression of NEIL1/3, RPA3 downregulated, and E3 ligase RNF8 upregulated. Expression of CDC25A upregulated in males and downregulated in females among exposed (p<0·05). |
| Guo et al (2019)72 | Cross-sectional: exposed town vs control town, China | 54 local adult residents aged 26–75 years | 58 local adult residents aged 26–75 years | PCBs, PBDEs, and NFR | ∑PCB=310 ng/g lipid vs 42 ng/g lipid, ∑PBDE=190 ng/g lipid vs 74 ng/g lipid, ∑NFR=350 ng/g lipid vs 110 ng/g lipid; all p<0·05). Lower expression of TRα=14 × 10−3vs 29 × 10, TRβ=0·47 × 10−3vs 0·32 × 10−3, and higher expression of ID1=4·2 × 10−3vs 3·2 × 10−3 (all p<0·05). High PCBs, PBDEs and NFRs exposures decrease expression of TRα, and increase expression of ID1 (p<0·05). |
| Oxidative damage | |||||
| Ni et al (2014)31 | Cross-sectional: exposed town vs control town, China | 126 pregnant women (mean age 26·05) | 75 pregnant women (mean age 25·45) | Lead, cadmium, chromium, and nickel | Umbilical cord blood lead=110 ng/mL vs 57 ng/mL, cadmium=2·50 ng/mL vs 0·33 ng/mL (p<0·001), no difference of nickel and chromium among groups (p>0·05). Umbilical cord blood 8-OHdG=162 ng/mL vs 154 ng/mL (p>0·05). 8-OHdG positively associated with cadmium (β=0·13, 95% CI 0·05 to 0·20), chromium (β=0·09, 95% CI 0·01 to 0·16), and nickel (β=0·21, 0·11 to 0·32; all p<0·05). |
| Zhou et al (2013)85 | Cross-sectional: exposed town vs reference town, China | 46 parturient women (mean age 27·82) | 44 parturient women (mean age 24·89) | Not assessed | Increased MDA, suppressed SOD in maternal serum, umbilical cord serum, placentas, and umbilical cord among exposed (p<0·05). GPx decreased in placentas and umbilical cord in exposed (p<0·05). MDA, SOD, and GPx in maternal serum associated with umbilical cord serum (r=0·90, r=0·86, r=0·85; all p<0·01), MDA, SOD, GPx in placentas associated with umbilical cords (r=0·89, r=0·96, r=0·77; all p<0·01). |
| Xu et al (2018)32 | Cross-sectional: e-waste recycling area, China | 118 preschool children aged: 3–6 years | None | Lead, cadmium, and mercury | Blood lead=7·43 μg/dL, blood cadmium=0·72 μg/L, blood mercury=11·13 μg/L, median 8-OHdG=407·79 ng/g cre, median mRNA expression level of hOGG1=0·038. Elevated blood lead (quartiles 2–4) had higher 8-OHdG (βQ2–Q4=0·31–0·36; p<0·05) than low blood lead (quartile 1). No correlation between blood cadmium and 8-OHdG (p>0·05), elevated blood mercury (quartile 2) correlated with 8-OHdG than low blood mercury (βQ2=0·23; p<0·05). |
| Li et al (2013)77 | Cross-sectional: exposed region vs reference region, China | 23 rural residents (mean age 32·6 years) | 28 rural residents (mean age 33·2 years) | PCBs, PBDEs, PBB, DP, HCB, β-HCH, and p,pʹ-DDE | PCBs=60·4 ng/g lipid vs 28·4 ng/g lipid, DP=9·0 ng/g lipid vs 2·8 ng/g lipid, PBB-153=0·55 ng/g lipid vs 0·25 ng/g lipid (all p<0·01). Increased ROS levels in WBC and NG, lower ROS in respiratory burst of NG among exposed (data not shown; p<0·001). Positive correlation between PCBs and ROS in WBC, NG (R=0·30 and R=0·31; p<0·05), inverse correlation between ROS in respiratory burst and PCBs (R=−0·45; p<0·01), no relation between ROS and PBDEs, DP, PBB153 (p>0·05). |
| Lu et al (2016)62 | Cross-sectional: e-waste exposed town vs rural reference vs urban reference town, China | 130 local residents aged 0·4–87 years | 24 rural residents and 22 urban residents aged 0·4–87 years | PAH | Urinary ∑10OH-PAHs=25·4 μg/g cre vs 11·7 μg/g cre vs 10·9 μg/g cre, 8-OHdG=16·2 μg/g cre vs 12·3 μg/g cre vs 11·6 μg/g cre, MDA=47·9 μg/g cre vs 36·1 μg/g cre vs 31·3 μg/g cre (all p<0·05). 8-OHdG significantly increased with ∑10OH-PAHs (β=0·35, 95% CI 0·21 to 0·49) and individual OH-PAHs (β=0·10–0·35; p<0·05), urinary 1-PYR correlated with MDA (r=0·28; p<0·01) in exposed group. |
| Lu et al (2017)84 | Cross-sectional: e-waste exposed town vs rural vs urban reference town, China | 175 local residents aged 0·4–87 years | 29 rural residents and 17 urban residents aged 0·4–87 years | Cl-mOPs and NCl-mOP metabolites | Urinary ∑Cl-mOPs=1·7 ng/mL vs 0·93 ng/mL vs 0·56 ng/mL (p<0·05), ∑NCl-mOPs=1·5 ng/mL vs 0·60 ng/mL (p<0·05 for exposed vs rural) vs 0·96 ng/mL, most abundant mOPs=BCEP (Cl-mOP) and DPHP (NCl-mOP) increased among exposed than rural reference (p<0·05). Significant association between 8-OHdG and BCEP (r=0·50), BCIPP (r=0·48), DBP (r=0·21), and DPHP (r=0·44) in exposed site (all p<0·05). |
| Yang et al (2015)63 | Cross-sectional: e-waste recycling site, China | 116 rural residents (mean age 36·9 years) | None | PAHs | 1-HO-PYR=0·57 μg/g cre, HO-PHEs=2·2 μg/g cre, HO-FLU=5·0 μg/g cre, HO-BPs=7·0 μg/g cre, HO-NAPs=16·6 μg/g cre. Urinary MDA and 8-OHdG=74·7 μg/g cre and 185 μg/g cre. Positive association between MDA and hydroxy-PAH (1-HO-PYR [β=0·40], HO-PHEs [β=0·48], HO-FLUs [β=0·35], HO-BPs [β=0·48], HO-NAPs [β=0·28]; all p<0·001), no correlation between 8-OHdG and hydroxy-PAH (p>0·05). |
| Zhang et al (2019)81 | Cross sectional: exposed vs reference village, China | 124 local residents aged 0·4–87 years | 22 local residents aged 0·4–87 years | PAEs | Urinary ∑mPAE=248 ng/mL vs reference (data not shown; p<0·05), higher mCMHP, mEHHP, mEHP, mMP, mEP in exposed group (p<0·05). Positive correlation between mECPP, mCMHP, mEHHP, mEHP, mCPP, mBP, miBP, mMP (8 of 11 mPAEs) and 8-OHdG (r=0·18–0·36; p<0·05). |
| Zhang et al (2019)33 | Cross sectional: exposed town vs rural reference, China | 139 local residents aged 0·4–87 years | 26 local residents aged 0·4–87 years | Lead, cadmium, mercury, arsenic, cobalt, manganese, copper, zinc, thallium, tin, antimony, selenium, and aluminium | Urinary lead=4·98 ng/mL vs 1·23 ng/mL, cadmium=2·12 ng/mL vs 1·33 ng/mL, copper=22·2 ng/mL vs 16·9 ng/mL, antimony=0·20 ng/mL vs 0·11 ng/mL, arsenic=46·6 ng/mL vs 62·0 ng/mL (p<0·05). Urinary 8-OHdG positively correlated with all metals (except manganese and aluminium) in exposed group (r=0·324–0·710; p<0·01), high correlation coefficient between highly toxic arsenic, mercury, lead, cadmium and 8-OHdG (r=0·45–0·61; p<0·01). |
| Zhang et al (2016)82 | Cross sectional: exposed villages vs rural reference village vs urban reference village, China | 116 local residents aged 0·4–87 years | 22 rural residents and 20 urban residents aged 0·4–87 years | BPA and 7 BPs | Urinary BPA=2·99 ng/mL vs 0·59 ng/mL vs 0·95 ng/mL (p<0·01), BPS=0·36 ng/mL vs 0·39 ng/mL (p>0·05 for exposed vs rural) vs 0·65 ng/mL, BPF=0·35 vs 0·09 (p<0·01 for exposed vs rural) vs 0·56 ng/mL, urinary 8-OHdG=8·00 ng/mL vs 6·84 ng/mL vs 7·31 ng/mL (p value not shown). 8-OHdG positively correlated with BPA (r=0·41) and BPS (r=0·39) in exposed (both p<0·001), no relation with BPF (p>0·05). |
PBDE=polybrominated diphenyl ether. lw=lipid weight. wt=weight. CAT=catalase. GSTO1=glutathione S transferase omega-1. Cyt=cytochrome. BDE=brominated diphenyl ether. TRF=terminal restriction fragment. cre=creatinine. T/S ratio=telomere/single copy gene ratio. OR=odds ratio. BAI1=brain-specific angiogenesis inhibitor 1. CTNNA2=catenin cadherin-associated protein. ALAD=δ-aminolevulinic acid dehydratase. MDA=malondialdehyde. PCB=polychlorinated bisphenol. IL=interleukin. TNF=tumor necrosis factor. LINE-1=long interspersed nuclear element-1. POP=persistent organic pollutant. hOGG1=human repair enzyme 8-oxoguanine DNA glycosylase. HCB=hexachlorobenzene. HCH=hexachlorocyclohexane. ROS=reactive oxygen species. TR=TH receptor. IDI=iodothyronine deiodinase. 8-OHdG=8-hydroxy-2ʹ-deoxyguanosine. SOD=superoxide dismutase. GPx=glutathione peroxidase. WBC=white blood cell. NG=neutrophil granulocytes. PBB=polybrominated biphenyls. Cl-mOPs=chlorinated organophosphate metabolites. NCl-mOPs=non-chlorinated organophosphate metabolites. BCEP=bis(2-chloroethyl) phosphate. BCIPP=bis(1-chloro-2-propyl) phosphate. DBP=dibutyl phosphate. DPHP=diphenyl phosphate. PYR=pyrene. HO-PYR=hydroxypyrene. HO-PHEs=hydroxyphenanthrenes. HO-FLU=hydroxyfluorenes. HO-BPs=hydroxybiphenyls. HO-NAPs=hydroxynaphthalenes. PAH=polycyclic aromatic hydrocarbons. ∑OHPAH=total hydroxylated PAH. ∑mPAE=phthalate esters metabolites. mCMHP=mono-[(2-carboxymethyl)hexyl] phthalate. mEHHP=5mono-(2-ethyl-5-hydroxyhexyl) phthalate. mEHP=mono-2-ethylhexyl phthalate. mMP=mono-methyl phthalate. mEP=mono-ethyl phthalate. mECPP=mono-(2-ethyl-5-carboxypentyl) phthalate. mBP=mono-n-butyl phthalate. miBP=mono-(2-isobutyl) phthalate. mCPP=mono (3-carboxypropyl) phthalate. BP=bisphenol.