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产前有机氯污染物暴露与全国出生队列精神分裂症风险的关系。

Prenatal organochlorine pollutant exposure and risk of schizophrenia in a national birth cohort.

机构信息

Department of Psychiatry, New York State Psychiatric Institute, Columbia University Irving Medical Center, New York, NY, USA.

Department of Health Security, Finnish Institute for Health and Welfare (THL), Kuopio, Finland.

出版信息

Neurotoxicology. 2023 Jul;97:47-52. doi: 10.1016/j.neuro.2023.05.010. Epub 2023 May 16.

Abstract

Non-genetic prenatal exposures have been associated with schizophrenia risk. However, the role of prenatal exposure to environmental neurotoxicants in offspring schizophrenia risk has been studied in only limited instances. Polychlorinated biphenyls (PCBs) and the pesticide metabolite p,p'-dichlorodiphenyl dichloroethylene (DDE) have been linked to neurodevelopmental outcomes, including impairments implicated in schizophrenia. To determine whether prenatal maternal levels of organochlorine pollutants including PCBs or DDE are associated with schizophrenia in the offspring, an investigation was conducted in the Finnish Prenatal Study of Schizophrenia (FIPS-S), a case-control study nested in a national birth cohort. Cases were born in 1987-1991 and had at least two diagnoses of schizophrenia (ICD-10 F20; ICD-9 295) or schizoaffective disorder (ICD-10 F25; ICD-9 295.7) recorded in the national Care Register for Health Care. Each case was individually matched to a control on sex, date of birth, and residence in Finland on the date of case diagnosis. In 500 case-control pairs, PCB congeners 74, 99, 118, 138, 153, 156, 170, 180, 183, 187, and some widespread organochlorine pesticides or their metabolites including DDE were measured in archived prenatal maternal sera using gas chromatography - high triple quadrupole mass spectrometry. Maternal total PCBs were quantified as the sum of concentrations of the measured congeners. Associations with schizophrenia were examined using conditional logistic regression. Maternal PCB or DDE levels greater than the 75th percentiles of the control distributions showed no evidence of association with offspring schizophrenia (PCBs: adjusted odds ratio (aOR) = 1.13, 95 % CI = 0.85-1.50), p = 0.41; DDE: aOR = 1.08, 95 % CI = 0.80-1.45; p = 0.63). Maternal levels of either pollutant dichotomized at the 90th percentile or considered as a continuous variable also did not show evidence for association with offspring schizophrenia. This study found a lack of evidence that prenatal maternal levels of the organochlorine pollutants DDE and PCBs are associated with offspring risk of schizophrenia.

摘要

非遗传的产前暴露与精神分裂症风险相关。然而,环境神经毒素产前暴露对后代精神分裂症风险的作用仅在有限的情况下进行了研究。多氯联苯(PCBs)和杀虫剂代谢物 p,p'-二氯二苯二氯乙烯(DDE)与神经发育结局有关,包括与精神分裂症有关的损伤。为了确定母体有机氯污染物包括 PCBs 或 DDE 的产前水平是否与后代的精神分裂症有关,在芬兰精神分裂症产前研究(FIPS-S)中进行了一项调查,这是一项嵌套在全国出生队列中的病例对照研究。病例出生于 1987-1991 年,在国家保健登记册中至少有两次精神分裂症(ICD-10 F20;ICD-9 295)或分裂情感障碍(ICD-10 F25;ICD-9 295.7)的诊断。每个病例都与性别、出生日期和病例诊断日期在芬兰的居住地点相匹配的对照进行个体匹配。在 500 对病例对照中,使用气相色谱-高三重四极杆质谱法在存档的产前母体血清中测量了 PCBs 同系物 74、99、118、138、153、156、170、180、183、187 和一些广泛存在的有机氯农药或其代谢物,包括 DDE。母体总 PCBs 的定量为所测量同系物浓度的总和。使用条件逻辑回归检查与精神分裂症的关联。母体 PCBs 或 DDE 水平高于对照分布的第 75 百分位数,与后代精神分裂症没有关联的证据(PCBs:调整后的优势比(aOR)=1.13,95%CI=0.85-1.50),p=0.41;DDE:aOR=1.08,95%CI=0.80-1.45;p=0.63)。母体污染物水平以第 90 百分位数或作为连续变量二分也没有证据表明与后代精神分裂症有关。本研究发现,没有证据表明母体产前有机氯污染物 DDE 和 PCBs 的水平与后代患精神分裂症的风险有关。

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