Title | Authors | Outcome | Conclusion | |
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PON1 and neurodevelopment in children from the CHAMACOS study exposed to organophosphate pesticides in utero | Eskenazi et al. [5] | Bayley MDIβ(95% CI) PON1-108 CC, reference (p < 0.01) CT, − 3.9 (− 6.6 to − 1.2) TT, − 5.7 (− 9.0 to − 2.5) PON1-192 RR, reference (p = 0.65) QR, − 0.5 (− 3.4 to − 2.4) QQ, 0.7 (− 2.6 to 4.0) Bayley PDI PON1-108 CC, reference (p=0.07) CT, − 1.4 (− 3.8 to − 1.0) TT, (− 5.7 to 0.2) PON1-192 RR, reference (p = 0.10) QR, 0.3 (− 2.2 to 2.9) (p = 1.0) QQ, 2.4 (− 0.5 to 5.4) (p = 1.0) CBCL PDD PON1-108 CC, reference (p = 0.14) CT, 1.5 (0.7 to 3.3) TT, 2.0 (0.8 to 5.1) PON1-192 RR, reference (p = 0.94) QR, (0.4 to 2.2) QQ, (0.4 to 2.4) | The PON1-108T allele in children associated with poorer Bayley MDI scores and with somewhat poor PDI scores. | |
Organophosphate pesticide exposure, PON1, and neurodevelopment in school-age children from the CHAMACOS study | Eskenazi et al. [21] | Mother PON1-108 KCPT ADHD [β(95%)] (at age 5), WISC PRI [β(95%)](age 7) CC, reference (p = 0.41), reference (p = 0.69) CT, 2.9 (− 1.9 to 7.8), − 2.6 (− 6.8 to 1.6) TT, 2.1 (− 3.6 to 7.9), − 2.8 (− 7.0 to 1.5) PON1 192 KCPT ADHD [β(95%)] (at age 5), WISC PRI [β(95%)](age 7) RR, reference (p = 0.86), reference (p = 0.65) QR, 2.1 (− 2.9 to 7.1), − 2.6 (− 7.0 to 1.7) QQ, − 0.5 (− 6.1 to 5.1), 1.0 (− 3.7 to 5.8) Child PON1 108 KCPT ADHD [β(95%)] (at age 5), WISC PRI [β(95%)](age 7) CC, reference (p = 0.88), reference (p = 0.52) CT, − 0.2 (− 4.9 to 4.6), − 0.5 (− 4.6 to 3.6) TT, 0.6 (− 5.4 to 6.5), − 1.8 (− 7.0 to 3.4) PON1 192 KCPT ADHD [β(95%)] (at age 5), WISC PRI [β(95%)](age 7) RR, reference (p = 0.96), reference (p = 0.21) QR, 5.0 (0.1 to 9.9), − 4.6 (− 9.0 to − 0.2) QQ, 0.1 (− 5.8 to 5.9), − 3.4 (− 8.5 to 1.7) | Maternal and child PON1 genotype was not related to performance on K-CPT or WISC; WISC scores were lowest in children and children of mothers who carried the PON1 108TT genotype. Maternal PON1 108 weakly modified the relationship of maternal DAPS and K-CPT score and WISC verbal IQ. PON1 genotype and enzyme levels may be related to performance on certain domains of neurodevelopment in school age children. | |
Urinary organophosphate insecticide metabolite concentrations during pregnancy and children's interpersonal, communication, repetitive, and stereotypic behaviours at 8 years of age: The home study | Millenson et al. [26] | PON1 108TT associated with [∑DAP] = β 2.5 point higher (95% CI − 4.9 to 9.8) PON1 108CT/CC associated with [∑DAP] = β 1.8 point decrease (95% CI − 5.8 to 2.2) (p = 0.54) PON1 192 modification by ∑DAP = not significantly different p = 0.89 | PON1 genotype did not modify association between DAP conc. And children social behaviour. | |
Paraoxonase gene variants are associated with autism in North America, but not in Italy: possible regional specificity in gene–environment interactions | D’Amelio et al. [27] | Caucasian-American PON1 108Zscore,pvalue TC, − 0.310, 0.7566 TT, 0.310 PON1 L55M ML, 2.435, 0.01489 MM, − 2.435 PON1 Q192R RQ, − 2.291, 0.02199 RR 2.291 Italian PON1 108 Z score, p value TC, 0.290, 0.772 TT, − 0.290 PON1 L55M ML, 0.079, 0.937 MM, − 0.079 PON1 Q192R RQ, 0.000, 1.000 RR, 0.000 | Caucasian-American, but not Italian, patients diagnosed with autism were more likely to carry the PON 1-108T allele and not the PON 192R allele, although not significant. | |
Paraoxinase 1 activities and polymorphisms in autism spectrum disorders | Pasca et al. [28] | PON1 Q192R [ASD(50), Control (30)],X2,p QQ, 26 (52.0%), 43 (50.6%); 0.02, 0.98 QR, 21 (42.0%), 37 (43.5%) RR, 3 (6%), 5 (5.9%) Q/R, 0.73/0.27, 0.72/0.28; 0.01, 0.90 PON1 L55M LL, 15 (30.0%), 31 (36.5%); 1.13, 0.56 LM, 30 (60.0%), 43 (50.6%) MM, 5 (10.0%), 11 (12.9%) L/M, 0.60/0.40; 0.62/0.38; 0.08, 0.77 | PON1 192 or PON1 55 allelic frequencies not significantly associated with enzymatic levels in ASD and non ASD control PON 1 Q192Q associated with POase activity PON1 enzyme activities are significantly decreased in ASD patients compared to healthy control, irrespective of PON1 polymorphism distribution. | |
Prenatal exposure to organophosphates, paraoxonase 1, and cognitive development in childhood | Engel et al. [29] | 1-year BSID-II Black/Hispanic PON1 192 (log10 β 95% CI) QQ, ∑DAP 5.72 (− 0.48 to 11.92), ∑DEP 3.69 (− 0.97 to 8.36), ∑DMP 2.76 (− 2.44 to 7.97) QR/RR, ∑DAP − 4.95 (− 7.81 to − 2.07) p<0.01, ∑DEP − 1.95 (− 5.36 to 1.47) p = 0.06, ∑DMP − 4.47 (− 7.05 to − 1.89) p = 0.02 | 2-year BSID-II all population PON1 192 (log10 β 95% CI) QQ, ∑DAP − 1.04 (− 6.06 to 3.99), ∑DEP − 0.55 (− 4.79 to 3.70), ∑DMP 0.12 (− 4.17 to 4.42) QR/RR, ∑DAP − 1.27 (− 4.40 to 1.84) p = 0.98, ∑DEP − 0.15 (− 3.51 to 3.21) p = 0.88, ∑DMP − 4.47 (− 3.27 to 2.30) p = 0.81 | Organophosphate negatively associated with cognitive development, particularly perceptual reasoning, starting at year and up to 9 year olds. Mothers carrying PON1 Q192R QR/RR genotype showed decreased mental development scores. |