Table 2.
Hormonal and immunological function resulting from exposure to electronic waste
| Exposure setting | Exposed population | Control population | Toxic chemicals | Health outcomes | |
|---|---|---|---|---|---|
| Hormonal | |||||
| Lv et al (2015)68 | Cross-sectional: exposed villages vs reference village, China | 64 pregnant women | 10 pregnant women | PCBs and PBDEs | Serum ∑PCBs=26·2 ng/g lw vs 14·0 ng/g lw, ∑PBDE8=9·77 ng/g lw vs 4·80 ng/g lw, PCB-153=8·30 ng/g lw vs 3·33 ng/g lw (p=not shown). PCBs, PCB-153, and PCB-138 negatively associated with lower TSH (r=−0·34, r=−0·38, r=−0·45; all p<0·05); no association between PCBs/PBDEs and TT3, TT4, FT3, FT4 (p>0·05). |
| Ben et al (2014)79 | Cross-sectional: exposed group (>20 years of living) vs control (<3 years), China | 48 mother–infant pairs (mothers aged ≥18 years) | 24 mother–infant pairs (mothers aged ≥18 years) | DPs | DP in maternal sera=13·5 ng/g lw vs 3·68 ng/g lw, placenta=4·27 ng/g lw vs 1·25 ng/g lw, cord blood=4·02 ng/g lw vs 2·03 ng/g lw (all p<0·05), strong correlations between DP concentrations in maternal sera and cord sera, maternal sera and placentas, placentas and cord sera (r>0·7; p<0·001). Lower TSH=1·76 μIU/mL vs 2·25 μIU/mL (p<0·05), no difference in TT3, TT4, FT3, FT4. DP levels associated with TT3 in maternal sera (syn-DP: r=0·37; anti-DP: r=0·36; p<0·05). |
| Zheng et al (2017)71 | Cross-sectional: exposed group (>20 years of living) vs control (<3 years), China | 48 paired mother–fetus | 24 paired mother–fetus | PBDEs | PBDE in serum=19·3 ng/g lw vs 8·13 ng/g lw, umbilical cord=6·84 ng/g lw vs 4·47 ng/g lw, placental tissue=2·20 ng/g lw vs 1·06 ng/g lw (p<0·05), major congener=BDE-209 and BDE-153. Significant association between BDE-153 and TT4 in exposed group (β=−0·15, 95% CI −0·23 to −0·07, R2= 0·531; p<0·001). |
| Xu et al (2013)61 | Cross-sectional: exposed city vs control city, China | 101 pregnant women (mean age 26·20 years) | 53 pregnant women (mean age 26·72 years) | PAHs and PBDEs | UCB ∑16PAHs=14·43 ppb vs 10·05 ppb, ∑PBDE=57·55 ng/g vs 8·23 ng/g lipid (both p<0·001). Increased placental IGF-1 and IGFBP-3 expression of mRNA (IGF-1: 0·23 vs 0·19 and IGFBP-3: 1·91 vs 0·68 (both p<0·05). Lower birthweight and Apgar score in exposed group. ∑PBDEs, ∑4 ring-PAHs and ∑16PAHs positively correlated with IGFBP-3 (β=0·44, β=0·34, and β=0·26, respectively; all p<0·01). BDE-154, BDE-209, and ∑5 ring-PAHs correlated with IGF-1 mRNA (β=0·23, β=0·24, and β=0·29, respectively; all p<0·05). |
| Xu et al (2014)29 | Cross-sectional: e-waste area, China | 162 children aged 4–6 years | None | PBDEs, lead, and cadmium | Serum PBDE=189·99 ng/g lipid, blood lead=14·53 μg/dL, blood cadmium=0·77 μg/L. Mean FT3=6·28 pmol/L, FT4=17·78 pmol/L, TSH=2·85 μIU/mL, IGF-1=510·79 ng/mL, IGFBP-3=60·97 ng/mL. ∑PBDEs negatively associated with FT3 (β=−0·19) and positively associated with TSH (β=0·27; both p<0·005). BDE-153 correlated with blood lead (β=0·19; p<0·05), no correlation between THs and blood lead or cadmium (p>0·05). |
| Xu et al (2014)69 | Cross-sectional: exposed town vs control town, China | 21 children aged 8 years | 24 children aged 8 years | PCBs, PBDEs, and PCDD/Fs | Serum ∑PCBs=40·56 ng/g lipid vs 20·69 ng/g lipid, ∑PBDEs=32·09 ng/g lipid vs 8·43 ng/g lipid (both p<0·001), PCDD/F=206 pg/g lipid vs 160 pg/g lipid (p>0·05). Elevated mean of FT3, TT3, TT4, ACTH, cortisol, GH, and lower FT4, TSH, no difference among groups (p>0·05). ∑PBDEs positively associated with ACTH (r=0·61; p<0·05), cortisol positively associated with TSH (r=0·50) and GH levels (0·51; both p<0·05). |
| Eguchi et al (2014)80 | Cross-sectional: exposed town vs non exposed rural site, Vietnam | 83 local residents, aged 10–64 years | 48 local residents, aged 10–64 years | Perchlorate (ClO4−) and thiocyanate (SCN−) | Serum perchlorate=0·116 ng/mL vs 0·086 ng/mL (p<0·05). Thiocyanate=2020 ng/mL, iodine=3·11 ng/mL, PEC=2·28 μmol/L, greater concentration among males (p<0·05). TT3=1·2 ng/mL vs 1·3 ng/mL, FT3=3·3 pg/mL vs 3·4 pg/mL (p<0·05), no correlation between THs and perchlorate/thiocyanate (p>0·05). Iodine significant positive predictor of FT3 (β=0·16), TT3 (β=0·19), and negative predictor of TSH (β=−0·45; all p<0·01) in males. |
| Eguchi et al (2015)67 | Cross-sectional: exposed town vs non-exposed rural site, Vietnam | 77 adult workers and residents (mean age 33 years) | 34 adult workers and residents (mean age 37 years) | PCBs, OH-PCB, PBDEs, MeO-PBDE, OH-PBDE, and BPh | Serum PCBs=420 pg/g vs 290 pg/g, OH-PCBs=160 pg/g vs 82 pg/g, PBDEs=290 pg/g vs 230 pg/g, and BPhs=300 pg/g vs 200 pg/g (all p<0·05). FT3=3·3 pg/g vs 3·5 pg/g, TT3=1·2 pg/g vs 1·3 pg/g, TT4=78 pg/g vs 85 pg/g (all p<0·05), FT4=1·3 pg/g vs 1·2 pg/g, TSH=1·4 pg/g vs 1·5 pg/g (both p>0·05). Positive correlation between FT4, FT3, TT3, TT4 and PCBs/OH-PCB, and negative correlation between PCB and TSH in females (all p<0·05). |
| Xu et al (2015)70 | Cross-sectional: exposed town vs control town, China | 40 local residents, aged 15–65 years | 15 local residents, aged 15–65 years | PCBs and PBDEs | Serum ∑PCBs=964 ng/g vs 68 ng/g (p<0·001), ∑PBDEs=139 ng/g vs 75 ng/g (p>0·05). FT3=4·72 pmol/L vs 5·64 pmol/L, FT4=14·98 pmol/L vs 18·67 pmol/L (both p<0·001), TSH=2·51 μIU/mL vs 1·80 μIU/mL (p>0·05). ∑PCBs negatively correlated with FT3 (r=−0·41) and FT4 (r=−0·39), no correlation between PBDEs and THs (p>0·05). |
| Guo et al (2019)72 | Cross-sectional: exposed town vs control town, China | 54 adult residents aged 26–75 years | 58 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). No mean difference of T3, T4, FT3, FT4, TSH among groups (p>0·05), TBG=18 μmol/L vs 20 μmol/L (p<0·05). PCB-28, 52, 101, 138, 153 negatively associated with FT4 (p<0·05), PBDEs negatively associated with T4(p<0·05). ∑NFR negatively associated with TSH (p<0·05) and TBG (p<0·05). Positive association between PBDE congener and T3 (BDE-85, BDE-99) and FT3 (BDE-47; all p<0·05). |
| Zheng et al (2017)73 | Cross sectional: e-waste recycling workers, China | 79 adult workers, aged 22–59 years | None | PBDEs, PCBs, and OH-PCB | Serum PCBs=2251 ng/g lipid, PBDEs=724 ng/g lipid, and OH-PCBs 418 ng/g lipid, no association between THs and PCBs/OH-PCBs (p>0·05), elevated T3 and T4 associated with certain PBDEs congeners (β=0·11–0·17; p<0·05). TH-regulated gene expression associated with certain PCB, OH-PCB, and mostly PBDE congeners (p<0·05) |
| Yan et al (2013)30 | Cross-sectional: e-waste dismantling area, China | 187 men aged 18–60 years | None | Lead | Blood lead=100·08 μg/L (≤30 years=98·55 μg/L, 31–45 years=100·23 μg/L, and 46–60 years=101·45 μg/L). FSH (≤30 years=5·64 mIU/mL, 31–45 years=11·51 mIU/mL, 46–60 years=15·32 mIU/mL), LH (≤30 years=4·59 mIU/mL, 31–45 years=4·90 mIU/mL, 46–60 years=5·96 mIU/mL), Tr (≤30 years=4823 mIU/mL, 31–45 years=4157 mIU/mL, 46–60 years=3562 mIU/mL). Blood lead associated with FSH (r=0·96), LH (r=0·92), and Tr levels (r=0·89; all p<0·01). |
| Guo et al (2018)74 | Ecological study: exposed town vs control town, China | 54 local residents, aged 26–75 years | 58 local residents, aged 26–75 years | NFR, PCBs, and PBDEs | Serum ∑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 among exposed group (all p<0·05). Female FSH=12 mIU/mL vs 55 mIU/mL (p<0·05). NFR (TBB, DPa, DBDPE) and PBDE (BDE-153, 154, 183) negatively associated with female FSH, male Tr positively associated with NFR (TBECH, BTBPE, DPa) and PBDE congener (BDE-47, 100, 153, 183, 207; p<0·05). |
| Zhou et al (2013)85 | Cross-sectional: exposed town vs reference town, China | 46 parturient women (mean age 27·82 years) | 44 parturient women (mean age 24·89 years) | Not assessed | Serum E2=2137 pg/mL vs 1549 pg/mL, umbilical cord E2=2758 pg/mL vs 2211 pg/mL, serum PROG=100 ng/mL vs 61 ng/mL, umbilical cord PROG=156 ng/mL vs 146 ng/mL (all p<0·05). mRNA of ERalpha, ERbeta increased in placenta and umbilical cord among exposed, mRNA of PROG decreased in placenta and umbilical cord among exposed (all p<0·05). |
| Immunological | |||||
| Cao et al (2018)40 | Cross-sectional: exposed town vs reference town, China | 62 preschool children aged 3–7 years | 56 preschool children aged 3–7 years | Lead | Blood lead=5·06 μg/dL vs 3·60 μg/dL (p<0·001). Higher percentage of CD4+ Tcm and CD8+ Tcm cells among exposed (geometric mean=25·79% vs 21·43% and 0·89% vs 0·62%, respectively; p<0·001). No difference in serum cytokines (IL-2, IL-7, IL-15) among groups. Blood lead positively associated with CD4+ Tcm (β=0·49; p<0·05) and marginal change in CD8+ Tcm (p<0·05). |
| Huo et al (2019)41 | Cross-sectional: exposed group vs reference group, China | 132 preschool children aged 2–7 years | 135 preschool children aged 2–7 years | Lead | Blood lead=6·51 μg/dL vs 4·41 μg/dL, erythrocyte lead=16·60 μg/dL vs 11·77 μg/dL (p<0·001). Reduced erythrocyte CD44 and CD58 expression (68·03% vs 76·15% and 40·76% vs 46·22%, respectively; p<0·01). Elevated erythrocyte lead associated with lower CD44 (BQ4 −5·44% [95% CI −9·11 to −1·73]) and CD58 (BQ4 −4·27% [−6·90 to −1·68]). Higher cytokines (IL-1β, IL12p70, IFN-γ, except IL-2). Elevated blood lead correlated with higher IL-12p70 (rs=0·20), IFN-γ (rs=0·22), and lower IL-2 (rs=−0·15), leukocyte count (rs=−0·12), lymphocyte ratio (rs=−0·16), LMR (rs=−0·18; all p<0·05). |
| Zhang et al (2016)42 | Cross sectional: exposed town vs reference town, China | 285 preschool children aged 3–7 years | 126 preschool children aged 3–7 years | Lead | Blood lead=6·00 μg/dL vs 3·92 μg/dL, and lower NK cells (CD3−CD56+, CD3−CD56brightCD16low/−, and CD3CD56dimCD16+), increased platelets, IL-1β and lower IL-2, IL-27, MIP-1α, MIP-1β concentration in exposed (all p<0·05), negative association between CD3−CD56bright CD16low/− and blood lead (β=−0·182; p<0·05). Blood lead correlated with platelet, neutrophil, monocyte (Rs=0·11, 0·14, and 0·12, respectively; p<0·05). IL-1β positively and IL-27 negatively associated with blood lead (Rs=0·16 and −0·31; p<0·05). |
PCB=polychlorinated bisphenol. PBDE=polybrominated diphenyl ether. lw=lipid weight. ∑PCBs=total PCB. ∑PBDE8=sum of eight congeners. TSH=thyroid stimulating hormone. TT3=total triiodothyronine. TT4=total thyroxine. FT3=free triiodothyronine. FT4=free thyroxine. DP=dechlorane plus. syn-DP=syn (or endo)-dechlorane plus. anti-DP=anti (or exo) dechlorane plus. PAH=polycyclic aromatic hydrocarbons. UCB=umbilical cord blood. ppb=parts per billion. IGF-1=insulin-like growth factor. IGFBP-3=IGF binding protein 3. TH=thyroid hormone. PCDD/F=polychlorinated dibenzo-p-dioxins and dibenzofurans. ACTH=adrenocorticotropic hormone. GH=growth hormone. PEC=perchlorate-equivalent concentrations. OH-PCB=hydroxylated PCB. MeO-PBDE=methoxylated PBDE. OH-PBDE=hydroxylated PBDE. BPh=bromophenols. FSH=follicle-stimulating hormone. LH=luteinising hormone. Tr=testosterone. NFR=new flame retardants. TBG=thyroxine-binding globulin. TBB=2-ethylhexyl 2,3,4,5-tetrabromobenzoate. DPa=dechlorane plus anti. DBDPE=1,2-bis(2,3,4,5,6-pentabromophenyl)ethane. TBECH=tetrabromoethylcyclohexane. BTBPE=1,2-bis(tribromophenoxy)-ethane. E2=oestradiol. PROG=progesterone. ERalpha=oestrogen receptor alpha. ERbeta=oestrogen receptor beta. CD4+Tcm=CD4+ central memory T cells. CD8+Tcm=CD8+ central memory T cells. BQ4=beta coefficient in quartile 4. IL=interleukin. IFN=interferon. LMR=lymphocyte-to-monocyte ratio. NK=natural killer. MIP=macrophage inflammatory protein.