Bj Wylie, S Kaali, L Duttweiler, Ka Ae-Ngibise, M Mujtaba, C Tawiah, E Gibson, Am Calafat, M Ospina, Dj Jack, O Agyei, Ag Lee, Dj Roberts, Ea Boamah-Kaali, P Factor-Litvak, Am Modest, R Hauser, Ba Coull, Kp Asante
Department of Obstetrics and Gynecology, Columbia University Medical Center, 622 West 168th Street, New York, NY 10032, United States; Department of Environmental Health Sciences, Columbia University Mailman School of Public Health, 722 West. 168th Street, New York, NY 10032, United States.
Kintampo Health Research Centre, Ghana Health Service, P.O. Box 200, Kintampo North Municipality, Ghana.
Environ Int. 2025 Feb;196:109292. doi: 10.1016/j.envint.2025.109292. Epub 2025 Jan 28.
Gestational pesticide exposure may negatively affect newborn outcomes. Prior results evaluating nonpersistent pesticides are inconsistent.
To examine associations between gestational exposure to nonpersistent pesticides and newborn outcomes and identify critical windows of susceptibility.
In a Ghanaian pregnancy cohort, we measured select biomarkers of organophosphate, pyrethroid, and herbicide pesticides in repeated urine samples (1-5/participant). We developed a new model for assessing critical windows of vulnerability from irregularly-timed measurements of nonpersistent pesticides, leveraging strengths from multiple informant and distributed lag models. We estimated associations of biomarker concentrations with newborn anthropometrics and gestational length, adjusting for confounders and exploring effect modification by infant sex and placental malaria.
1,211 pregnant women contributed 3,786 gestational urinary samples. In models assuming constant associations with exposures across pregnancy, in a given week a doubling of 3-phenoxybenzoic acid (pyrethroid biomarker) was associated with a -15.8 g difference in birth weight (95 % CI:-28.1,-3.6), and a doubling of the 2,4-dichlorophenoxyacetic acid (2,4-D, herbicide biomarker) was associated with an 11.1 g increase in birth weight (95 % CI:1.0,21.1). In time-varying models, significant associations were identified for pyrethroid exposure measured between weeks 16-27, and for 2,4-D exposure measured during weeks 25-33. Organophosphates were not associated with birth weight. No associations were found for birth length or head circumference for any pesticide. In constant association models, a doubling of weekly 2,4-D was associated with a 0.05 week increase in gestational length (95 %CI:0.01,0.09); no associations were found with other biomarkers.
We identified associations between gestational exposure to nonpersistent pesticides and both birth size and gestational length. Extending multiple informant models to account for the complex data structure allowed us to discern effects in opposing directions by distinct pesticide classes. While estimated effects for a given week were modest, prolonged or repeated exposures could result in larger cumulative impacts.
孕期接触农药可能会对新生儿结局产生负面影响。先前评估非持久性农药的结果并不一致。
研究孕期接触非持久性农药与新生儿结局之间的关联,并确定关键的易感性窗口期。
在一个加纳的妊娠队列中,我们在多次采集的尿液样本(每位参与者1 - 5次)中测量了有机磷、拟除虫菊酯和除草剂农药的特定生物标志物。我们开发了一种新模型,用于从不定期测量的非持久性农药数据中评估关键的易损窗口期,该模型借鉴了多种信息来源模型和分布滞后模型的优势。我们估计了生物标志物浓度与新生儿人体测量指标和妊娠时长之间的关联,对混杂因素进行了调整,并探讨了婴儿性别和胎盘疟疾对效应的修饰作用。
1211名孕妇提供了3786份孕期尿液样本。在假设孕期各阶段接触农药的关联恒定的模型中,在给定的一周内,3 - 苯氧基苯甲酸(拟除虫菊酯生物标志物)浓度翻倍与出生体重相差 - 15.8克相关(95%置信区间:- 28.1,- 3.6),2,4 - 二氯苯氧乙酸(2,4 - D,除草剂生物标志物)浓度翻倍与出生体重增加11.1克相关(95%置信区间:1.0,21.1)。在时变模型中,确定在第16 - 27周测量的拟除虫菊酯暴露以及在第25 - 33周测量的2,4 - D暴露存在显著关联。有机磷与出生体重无关。未发现任何农药与出生身长或头围存在关联。在关联恒定模型中,每周2,4 - D浓度翻倍与妊娠时长增加0.05周相关(95%置信区间:0.01,0.09);未发现与其他生物标志物存在关联。
我们确定了孕期接触非持久性农药与出生大小和妊娠时长之间的关联。扩展多种信息来源模型以考虑复杂的数据结构,使我们能够辨别不同农药类别在相反方向上的效应。虽然给定一周内的估计效应较小,但长期或反复接触可能会导致更大的累积影响。