A Review of Recent Studies on Bisphenol A and Phthalate Exposures and Child Neurodevelopment
Abstract
:1. Introduction
Brief Review of Studies Prior to the Past 5 Years
2. Methods
2.1. Bisphenol A and Neurodevelopment
2.2. Behavioral Outcomes (Pre-, Postnatal and Concurrent Exposure)
2.3. Cognitive Development (Prenatal Exposure)
2.4. Psychomotor Development (Prenatal and Concurrent Exposure)
2.5. Exposure Assessment of Bisphenol A
2.6. Phthalates and Neurodevelopment
2.7. Mechanisms Linking Bisphenol A, Phthalate Exposure, and Neurodevelopment
2.7.1. Thyroid Disruption
2.7.2. Brain Function and Structure Disruption
2.7.3. Endocrine and Metabolic Disruption
2.8. Oxidative Stress
2.9. Epigenetics
3. Future Directions
4. Conclusions
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Conflicts of Interest
Human and Animal Rights and Informed Consent
References
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Reference | Study Design | Location | Sample Size | Age | Exposure Levels/Specimen | Test Tool | Main Findings |
---|---|---|---|---|---|---|---|
Casas et al. [21] | Longitudinal | Spain | 438 | 1, 4, 7 y | 2.6 μg/g Cr (GM)/1st and 3rd trimester maternal urine | BSID-I MSCA DSM-IV CPRS SDQ | Prenatal exposure does not affect cognitive development up to age 4 years. Associations are observed with psychomotor development (β= −4.28, 95% confidence interval (CI): −8.15, −0.41) and ADHD-related symptoms (IRR(Incidence rate ratio) = 1.72; 95% CI: 1.08, 2.73) at early ages, but these do not appear to persist until later ages. |
Roen et al. [22] | Longitudinal | US | 250 | 7–9 y | 1.9 μg/L (GM)/3rd trimester maternal urine 3.2 μg/L (GM)/child urine | CBCL | High prenatal concentration was associated with increased internalizing (β = 0.41) and externalizing (β = 0.40) composite scores and with their corresponding individual syndrome scales (boys). High postnatal concentration was associated with increased behaviors on both internalizing (β = 0.30) and externalizing (β = 0.33) composite scores and individual sub scores (girls). |
Perera et al. [23] | Longitudinal | US | 241 | 10–12 y | 1.93 μg/L (GM)/3rd trimester maternal urine 5.28 μg/L (GM)/child urine | RCMAS CDRS | Prenatal exposure was associated with more symptoms of anxiety and depression (β = 2.83) (boys). |
Lim et al. [24] | Longitudinal | Korea | 304 | 4 y | 2.0 μg/g Cr (mean)/mid-pregnancy urine 4.9 μg/g Cr (mean)/child urine | K-SCQ | Pre and postnatal exposure were associated with increase in social impairment (β = 58.4%; 95% CI: 6.5, 135.8, β = 11.8%; 95% CI: 0.6, 24.3, respectively) (girls). |
Braun et al. [25] | Longitudinal | US | 346 | 1–8 y | 2.0 μg/g Cr (median)/maternal urine at 16 and 26 weeks | BASC-2 BSID-II WPPSI-III WISC-IV | Prenatal exposure was associated with more externalizing behaviors (β = 5.9; 95% CI: 1.1, 11) (girls). |
Lin et al. [26] | Longitudinal | Taiwan | 208 (2 y) 148 (7 y) | 2 y 7 y | 3.2–3.3 ng/mL (median)/cord blood | CDIIT WICS-IV | Prenatal exposure had adverse effects on full-scale IQ and verbal comprehension index (boys). Prenatal exposure had adverse effects on full-scale IQ, perceptual reasoning index, and working memory index (girls). |
Stacy et al. [27] | Longitudinal | US | 228 | 8 y | 2.1 ng/mL (median)/maternal urine1.6 ng/mL (median)/child urine | BASC-2 WISC-IV BRIEF | Prenatal exposure was associated with more externalizing behaviors (β = 6.2, 95% CI: 0.8, 11.6) (girls). Concurrent exposure was associated with more externalizing behaviors (β = 3.9, 95% CI: 0.6, 7.2) (boys). |
Minatoya et al. [28] | Longitudinal | Japan | 285 | 6 m 18 m 3.5 y | 0.051 ng/mL (median)/cord blood | BSID-II K-ABC CBCL | No association between prenatal exposure and child mental or psychomotor ability but was positively associated with development problems score (β = 2.60, 95% CI: 0.15, 5.06). |
Braun et al. [29] | Longitudinal | Canada | 812 | 3 y | 0.8 ng/mL (median)/maternal urine at 12.1 weeks | WPPSI-III BRIEF-P BASC-2 SRS-2 | Prenatal exposure was associated with poorer working memory and more internalizing and somatizing behaviors (β = 0.5; 95% CI: −0.1, 1.1, β = 0.6; 95% CI: 0.0, 1.2, respectively) (boys). Prenatal exposure was associated with poorer SRS-2 scores (β = 0.3; 95% CI: 0, 0.7). |
Braun et al. [30] | Longitudinal | US | 198 | 8 y | 2.0 μg/g Cr (median)/maternal urine at 16 and 26 weeks | VMWM | Prenatal exposure was not associated with VMWM performance. |
Minatoya et al. [31] | Longitudinal | Japan | 458 | 5 y | 0.062 ng/mL (median)/1st trimester maternal serum | SDQ | No significant association of prenatal exposure. |
Pan et al. [32] | Longitudinal | China | 368 (12 m) 296 (24 m) | 12 m 24 m | 1.05 μg/g Cr (median)/maternal urine at delivery | DQ | Prenatal exposure was adversely associated with the adaptive domain DQs (boys and girls) (β = −1.43; 95% CI: −2.30, −0.56), and the social domain DQs (girls) at 12 mo, as well as with the language domain (girls) at 24 mo (β = −1.69; 95% CI: −3.23, −0.15). |
Jensen et al. [33] | Longitudinal | Denmark | 535 (MB-CDI) 658 (CBCL) | 21 m 2–7 y | 1.2 ng/mL (median)/3rd trimester maternal urine | MB-CDI CBCL | Prenatal exposure adversely associated with vocabulary score (boys). BPA exposure in the highest tertile had OR = 3.70; 95% CI: 1.34–10.21. |
Jiang et al. [34] | Longitudinal | China | 456 | 2 y | 1.13 μg/L (median, average)/1st, 2nd, 3rd trimester maternal urine | BSID-I | Increase in BPA concentrations was related to lower MDI scores only in the 2nd trimester (β = −2.87, 95 % CI: −4.98, −0.75). |
Guo et al. [35] | Longitudinal | China | 326 | 7 y | 2.78 μg/L (GM)/Maternal urine | C-WISC | Prenatal exposure was significantly negatively associated with FIQ (β = −1.18, 95% CI: −2.21, −0.15). |
England-Mason et al. [36] | Longitudinal | Canada | 312 | 2 and 4 y | 1.64 μg/g Cr (GM)/3rd trimester maternal urine 1.11 μg/g Cr (GM)/postpartum maternal urine | BRIEF-P | Higher concentrations of maternal BPA at 3-month postpartum were associated with increasing difficulties in inhibitory self-control and emergent metacognition from age 2 to 4 (girls). |
Freire et al. [37] | Longitudinal | Spain | 191 | 4–5 y | 1.30 ng/g (median)/placenta | MSCA | Prenatal exposure was associated with greater ORs of scoring lower in the verbal (OR = 2.78, 95% CI: 1.00–5.81) and gross motor (OR = 1.75, 95% CI: 1.06–9.29). |
Perez-Lobato et al. [38] | Cross-sectional | Spain | 300 | 9–11 y | 4.76 μg/L (median)/child urine | CBCL/6-18 | Concurrent exposure was associated with worse behavioral scores. Children with the highest BPA had more somatic complaints (β = 2.35; 95% CI: 0.25, 4.46) and social (β = 1.71; 95% CI: 0.19, 3.22) and thought problems (β = 2.58; 95% CI: 0.66, 4.51). |
Arbuckle et al. [39] | Cross-sectional | Canada | 1080 | 6–11 y | 1.31 μg/L (GM)/child urine | SDQ | Concurrent exposure was not associated with SDQ score but was associated with taking psychotropic medications (OR = 1.59; 95% CI: 1.05–2.40). |
Tewar et al. [40] | Cross-sectional | US | 460 | 8–15 y | 3.9μg/L(median)/child urine | ADHD diagnosis | Concurrent exposure was associated with ADHD and the association was stronger in boys (OR = 10.9; 95% CI: 1.4–86.0). |
Li et al. [41] | Case-control | China | 215 (case) 253 (control) | 6–12 y | Case 4.63 μg/g Cr Control 1.71 μg/g Cr (mean)/child urine | ADHD diagnosis | Concurrent exposure may be related to ADHD. (OR = 4.58; 95% CI: 2.84–7.37 boys, OR = 2.83; 95% CI: 1.17–6.84 girls). |
Stein et al. [42] | Case-control | US | 46 (ASD) 52 (control) | 10 y (mean) | Case 11.18 ng/mL Control 6.58 ng/mL (median)/child urine | ASD diagnosis | Concurrent exposure was associated with ASD. Total BPA was 3 times greater with the ASD group (p < 0.001). |
Rahbar et al. [43] | Case-control | US | 30 (ASD) 10 (control) | 2–8 y | Case 1.33 µg/g Cr Control 0.93 µg/g Cr (mean)/child urine | ASD diagnosis | Controls had lower bisphenol A levels. |
Tsai et al. [44] | Case-control | Taiwan | 130 (ADHD) 68 (control) | 6–12 y | Not provided. | ADHD diagnosis | No significant difference of urinary BPA levels between case and control groups. |
Reference | Study Design | Location | Sample Size | Age | Exposure Level/Specimen | Test Tool | Main Findings |
---|---|---|---|---|---|---|---|
Lien et al. [45] | Longitudinal | Taiwan | 122 | 8 y | MBP = 66.88 μg/g Cr MEOHP = 13.59μg/g Cr MEHP =16.93 μg/g Cr (GM)/3rd trimester maternal urine | CBCL | Prenatal DEHP and DBP exposures were associated with externalizing domain behavior problems. MBP (β = 4.29; 95% CI: 0.59, 7.99), MEOHP (β = 3.74; 95% CI: 1.33, 6.15), and MEHP (β = 4.28; 95% CI: 0.03, 8.26). |
Gascon et al. [46] | Longitudinal | Spain | 367 | 1, 4, 7 y | MBzP = 11.9 μg/g CrΣ4DEHP = 99.8 μg/g Cr (median)/maternal urine at 12 and 32 weeks of gestation | BSID-I MSCA DSM-IV CPRS SDQ | No associations between prenatal exposure and cognitive and psychomotor scores at the age of 1 and 4 years, except for MBzP levels and lower psychomotor scores (β = −1.49; 95% CI: −2.78, −0.21). Prenatal DEHP exposure was associated with increased social competence scores at 4 years (β = 2.00; 95% CI: 0.22, 3.79) and with reduced ADHD symptoms at age 4 and 7 years (IRR = 0.84; 95% CI: 0.72, 0.98, IRR = 0.83; 95% CI: 0.71, 0.95, respectively). Prenatal DEP exposure was associated with a reduced risk of inattention symptoms at 4 years (IRR = 0.88; 95% CI: 0.80, 0.97). |
Minatoya et al. [47] | Longitudinal | Japan | 328 | 6 m 18 m | DEHP = 8.81 ng/mL (median)/maternal blood | BSID-II | Prenatal DEHP exposure was not associated with mental and psychomotor development. |
Messerlian et al. [48] | Longitudinal | US | 166 | 2–9 y | ΣDEHP = 60.7 ng/mL MiBP = 5.9 ng/mL (GM)/maternal urine before pregnancy | BASC-2 | Pre-conceptional exposure to DEHP was associated with a decrease in internalizing behavior scores (β = −2.0; 95% CI: −3.2, −0.7). MiBP was positively associated with externalizing behaviors (β = 1.7; 95% CI: 0.3, 3.2) (boys). |
Huang et al. [49] | Longitudinal | Taiwan | 204 | 3–12 y | MEOHP = 32.2 μg/g Cr MnBP = 46.2 μg/g Cr MiBP = 24.3 μg/g Cr (median)/child urine | WISC-IV WPPSI-R | Postnatal exposure to DEHP and DnBP affect intellectual development, particularly language learning or expression ability (β = −11.92; 95% CI: −22.52, −1.33, β = −10.95; 95% CI: −20.74, −1.16, respectively). |
Doherty et al. [50] | Longitudinal | US | 276 | 24 m | MnBP = 33.0 μg/L MnBP = 5.6 μg/L MCPP = 2.9 μg/L (GM)/31st weeks maternal urine | BSID-II | Prenatal exposure to DnOP and DBP were associated with lower MDI scores (girls) and improved scores (boys). |
Minatoya et al. [31] | Longitudinal | Japan | 458 | 5 y | MECPP = 0.20 ng/mL (median)/maternal serum | SDQ | Possible association between prenatal DEHP exposure and increased risk of conduct problems (OR = 2.78, 95% CI 1.36–5.68). |
Singer et al. [51] | Longitudinal | US | 204 (12mo) 279 (24 m) | 12 m/24 m | 3rd trimester Maternal urine | IBQ (12mo) TBAQ (24mo) | Prenatal exposure to DnOP and BBzP were associated with social fear (β = 0.3; 95% CI: −0.1, 0.6, β = 0.3; 95% CI: 0.0, 0.5, respectively) and lower pleasure β = −0.2; 95% CI: −0.4, −0.1, β = −0.1; 95% CI: −0.2, 0.0, respectively) at 24 mo. |
Braun et al. [30] | Longitudinal | US | 198 | 8 y | MnBP = 24 μg/g Cr (median)/maternal urine at 16 and 26 weeks | VMWM | Prenatal higher MnBP was associated with longer time (1.7 s; 95% CI: −0.7, 4.1) and shorter distance (−1.7 units; 95% CI: −2.8, −0.5) (girls), and with shorter time (−3.0 s; 95% CI: −5.6, −0.4) (boys). |
Kim et al. [52] | Longitudinal | Korea | 140 | 1–2 y | MEP = 11.9 μg/g Cr (median)/maternal urine at delivery MEHP = 2.5 μg/L (median)/breast milk 30days after delivery | BSID-II SMS CBCL | Prenatal DEP exposure was associated with early mental (β = −2.40; 95% CI: −4.39, −0.40), psychomotor (β = −2.25; 95% CI: −4.03, −0.47), and social development (β = −2.54; 95% CI: −4.44, −0.65). Postnatal exposure to DEHP was inversely associated with mental (β = −5.60; 95% CI: −11.05, −0.14). |
Bornehag et al. [53] | Longitudinal | US, Sweden | 963 (Sweden) 370 (US) | 30 m (Sweden) 37 m (US) | MBP = 69.4 (Sweden), 6.5 (US) ng/mL MBzP = 16.1 (Sweden), 3.4 (US) ng/mL (GM)/maternal urine at 10.9 weeks | Language Development Assessment | Prenatal exposure to DBP (OR =1.29; 95% CI: 1.03, 1.63) and BBzP (OR = 1.14; 95% CI: 1.00, 1.31) was associated with language delay. |
Hyland et al. [54] | Longitudinal | US | 334 | 7–16 y | ΣLMW = 1.5 nmol/mL (GM)/maternal urine | BRIEF WCST WICS-IV ENI NEPSY-II SRS-2 BASC-2 SRP CADS CPT-II | Prenatal exposure to LMW phthalates was associated with more self-reported hyperactivity (β = 0.8; 95% CI: 0.1, 1.4), attention problems (β = 1.5; 95% CI: 0.7, 2.2), and anxiety (β = 0.9; 95% CI: 0.0, 1.8) at age 16. |
Jankowska et al. [55] | Longitudinal | Poland | 134 | 7 y | MEP = 19.4 μg/g Cr MnBP = 4.1 μg/g Cr Oxo-MEHP = 1.6 μg/g Cr (median)/maternal urine at 3rd trimester | SDQ IDS | Prenatal exposure to DEP was associated with an increased risk of peer relationship problems (OR = 2.7). Prenatal DEP and DnBP exposure were negatively associated with fluid intelligence (β = −5.2, β = −4.9, respectively) and cognition (β = −4.2, β = −4.0, respectively) while the oxo-MEHP level was positively associated (β = 3.6, β = 2.9, respectively). |
Qian et al. [56] | Longitudinal | China | 476 | 2 y | ΣLMW = 547.96 nmol/L ΣHMW = 107.29 nmol/L (median)/maternal urine | BSID-II | Prenatal exposure to DBP was associated with decreased PDI scores (β = −1.89, 95% CI: −3.63, −0.15). A negative association between exposure to HMW phthalates and PDI scores (girls), as well as a positive association (boys), were found. |
Chen et al. [57] | Longitudinal | Taiwan | 122/96/78 | 8,11, 14 y | DEHP = 4.54 μg/kg_bw/day/maternal urine at 3rd trimester | CBCL | Prenatal DEHP exposure was associated with increased CBCL scores (2.02 for internalizing, 2.88 for externalizing problems). |
Dong et al. [58] | Longitudinal | China | 138 | 9 m | MMP = 29.98 μg/g Cr MEP = 52.45 μg/g Cr MiBP = 127.49 μg/g Cr MnBP = 115.08 μg/g Cr MEHP = 23.67 μg/g Cr (GM)/maternal urine | ASQ-3 | Prenatal exposure was mostly associated with DD. MMP, MEP, MiBP and MnBP levels were associated with increased ORs of DD of all domains (boys), and LMW phthalate and DEHP were associated with increased ORs of DD of most domains (girls). |
Daniel et al. [59] | Longitudinal | US | 411 | 7 y | MnBP = 13.3 ng/mL MiBP = 9.1 ng/mL MnBP = 37.4 ng/mL MEOHP = 18.4 ng/mL MEHHP = 22.1 ng/mL (GM)/3rd trimester maternal urine | CBCL, CPRS | Increases in in anxious-shy behaviors were associated with prenatal exposure to MBzP (MR = 1.20, 95% CI 1.05–1.36) and MiBP (MR = 1.22, 95% CI 1.02–1.47) (boys). Increases in perfectionism were associated with MBzP (MR = 1.15, 95% CI 1.01–1.30), decreased hyperactivity was associated with MEOHP (MR = 0.83, 95% CI 0.71–0.98) and MEHHP (MR = 0.85, 95% CI 0.72–0.99) (girls). Increases in psychosomatic problems were associated with MiBP (MR = 1.28, 95% CI 1.02–1.60), and MnBP (MR = 1.28, 95% CI 1.02–1.59) (boys and girls). |
Li et al. [60] | Longitudinal | US | 314 | 2, 3, 4, 5, 8 y | Values were provided as log10-transformed creatinine-standardized form/maternal urine at 16 and 26 weeks and child urine | BASC-2 | Prenatal MCPP exposure was associated with more problem behaviors (internalizing: β = 0.9, 95% CI = −0.1, 1.9; externalizing: β = 1.0, 95% CI = −0.1, 2.0; BSI: β = 1.1, 95% CI = 0.1, 2.1). The weighted childhood phthalate index was associated with more problem behaviors (internalizing: β = 1.5, 95% CI = −0.2, 3.1; externalizing: β = 1.7, 95% CI = 0.1, 3.5; BSI: β = 1.7, 95% CI = 0.2, 3.2); MBzP, MCNP, and MEP largely contributed to these associations. |
Torres-Olascoaga et al. [61] | Longitudinal | Mexico | 218 | 48 m | MEHP = 7.8–9.5 ng/L MEHHP = 30.5–32.5 ng/L MEOHP = 16.3–19.4 ng/L MECPP = 46.7–55.4 ng/L MBzP = 4.6–7.3 ng/L MCPP = 1.6–2.4 ng/L (mean)/1st, 2nd, 3rd trimester maternal urine | MSCA | Inverse association was observed between the prenatal exposure to HMW phthalates. |
Jankowska et al. [62] | Cross-sectional | Poland | 250 | 7 y | DnBP = 62.6 μg/L MEP = 42.0 μg/L (median)/child urine | SDQ IDS | Prenatal exposure to DMP and DnBP were associated with higher total difficulties scores (β = 1.5; 95% CI: 0.17, 2.7, β = 1.5, 95% CI: 0.25, 2.8, respectively). Prenatal DnBP and DMP exposures were negatively associated with fluid IQ (β = −0.14, 95% CI: −0.29, 0.0041) and crystallized IQ (β = −0.16, 95% CI: −0.29, −0.025). Prenatal DMP (β = −0.17; 95% CI: −0.31, −0.033), DEP (β = −0.16; 95% CI: −0.29, −0.018), and DnBP (β = −0.14; 95% CI: −0.28, 0.0012) exposure were associated with mathematical skills. |
Won et al. [63] | Cross-sectional | Korea | 1723/867 | 6–18 y | MBzP = 4.82 μg/g Cr MnBP = 40.84 μg/g Cr MECPP = 32.10 μg/g Cr MEOHP = 15.95 μg/g Cr MEHHP = 21.76 μg/g Cr (GM)/child urine | CBCL ARS | Concurrent exposure to DnBP was associated with social (β=0.60; 95% CI: 0.15, 1.05), thought (β=0.55; 95% CI: 0.08, 1.03), and attention problems (β=0.68; 95% CI: 0.21, 1.14). Higher levels of MnBP, MEOHP, and MEHHP were associated with an increase in thought problems (girls). Among children aged 6–11 years, positive associations between the MnBP, MECPP, MEOHP, and MEHHP levels and social problems, as well as between the MnBP, MEOHP, and MEHHP levels and attention problems, were observed. |
Arbuckle et al. [39] | Cross-sectional | Canada | 1080 | 6–11 y | MBzP = 21.23 μg/L (GM)/child urine | SDQ | Concurrent BBzP exposure was associated with emotional symptoms (OR = 1.38; 95% CI: 1.09, 1.75) (girls). |
Philippat et al. [64] | Case-control | US | 50 (ASD) 27 (DD) 68 (TD) | 24–60 m | DEHP = 187 μg/g BBzP = 13 μg/g DEP = 1 μg/g DBP = 10 μg/g (median)/home dust | VABS ABC MSEL | Concurrent DEHP and BBzP levels in indoor dust were higher at homes of DD children (OR = 2.10; 95% CI: 1.10, 4.09, OR = 1.40; 95% CI: 0.97, 2.04, respectively). Among ASD and DD, higher indoor dust levels of DEP and DBP were associated with greater hyperactivity-impulsivity and inattention (boys). |
Park et al. [65] | Case-control | Korea | 180 (ADHD) 438 (control) | 6–15 y | MEHP = 45.60 μg/g Cr MEOP = 43.82 μg/g Cr MBP = 68.03 μg/g Cr (GM)/child urine | ADHD-RS CGI-S DBDS DSM-IV CBCL CPT brain cortical thickness | Concurrent DEHP levels were higher with ADHD than without ADHD (boys). Concurrent DBP levels were higher in the combined or hyperactive-impulsive subtypes compared to the inattentive subtype and was positively correlated with the severity of externalizing symptoms. Concurrent DEHP levels were negatively correlated with cortical thickness. |
Hu et al. [66] | Case-control | China | 225 (ADHD) 225 (control) | 6–13 y | MEHP = 6.72 ng/mL MEHHP = 30.23 ng/mL MEOHP = 14.94 ng/mL (median)/child urine | SNAP-IV CBCL | Concurrent DEHP levels were dose-dependently associated with ADHD (ORs = 2.35–3.04) and co-occurring ODD (ORs = 3.27–4.44) and related to attention problems, aggressivity, depression, and externalizing and internalizing behaviors. |
Rahbar et al. [43] | Case-control | US | 30 (ASD) 10 (control) | 2–8 y | (ASD) MEHHP = 14.94 μg/g Cr (control) MEHHP =11.08 μg/g Cr (mean)/Child urine | ASD diagnosis | Controls had lower MEHHP (26%) and higher MBP (50%) levels compared to the cases. |
Engel et al. [67] | Nested case-control | Norway | 297 (ADHD) 553 (control) | born 2003–2008 | (ADHD) ΣDEHP = 0.31 μmol/L (control) ΣDEHP = 0.27 μmol/L (GM)/child urine | ADHD diagnosis | Prenatal exposure to DEHP was associated with increased the risk of ADHD (OR = 2.99; 95% CI: 1.47, 5.49). |
Shin et al. [68] | Case-control | US | 46 (ASD) 55 (Non-TD) 100 (TD) | 3 y | (ASD) ΣDEHP = 0.14 μmol/L (Non-TD) ΣDEHP = 0.19 μmol/L (TD) ΣDEHP = 0.17 μmol/L (median)/maternal urine during pregnancy | clinical diagnosis | Prenatal exposure to DEP was associated with an increased risk of Non-TD (RRR = 1.38; 95% CI: 1.01, 1.90). ASD risk was inversely associated with prenatal exposure to DiBP, DMP, and DiNP; however, among mothers who did not take prenatal vitamins, (MiBP, RRR = 0.44; 95% CI: 0.21, 0.88), (MCPP, RRR = 0.41; 95% CI: 0.20, 0.83) (MCOP, RRR = 0.49; 95% CI: 0.27, 0.88), the Non-TD risk was positively associated with DnOP, MCOP and DDP exposure (MCPP, RRR = 5.09; 95% CI: 2.05, 12.6), (MCOP, RRR = 1.86; 95% CI: 1.01, 3.39), (MCNP, RRR = 3.67; 95% CI: 1.80, 7.48). Prenatal exposure to DEP, DBP, DiNP, DMP, and DEHP were positively associated with Non-TD risk (boys). |
Tsai et al. [44] | Case-control | Taiwan | 130 (ADHD) 68 (control) | 6–12 y | Not provided. | ADHD diagnosis | ADHD group demonstrated higher MnBP (p = 0.014) (boys). |
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Minatoya, M.; Kishi, R. A Review of Recent Studies on Bisphenol A and Phthalate Exposures and Child Neurodevelopment. Int. J. Environ. Res. Public Health 2021, 18, 3585. https://doi.org/10.3390/ijerph18073585
Minatoya M, Kishi R. A Review of Recent Studies on Bisphenol A and Phthalate Exposures and Child Neurodevelopment. International Journal of Environmental Research and Public Health. 2021; 18(7):3585. https://doi.org/10.3390/ijerph18073585
Chicago/Turabian StyleMinatoya, Machiko, and Reiko Kishi. 2021. "A Review of Recent Studies on Bisphenol A and Phthalate Exposures and Child Neurodevelopment" International Journal of Environmental Research and Public Health 18, no. 7: 3585. https://doi.org/10.3390/ijerph18073585
APA StyleMinatoya, M., & Kishi, R. (2021). A Review of Recent Studies on Bisphenol A and Phthalate Exposures and Child Neurodevelopment. International Journal of Environmental Research and Public Health, 18(7), 3585. https://doi.org/10.3390/ijerph18073585