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. 2024 Jul 1;252(Pt 1):118822.
doi: 10.1016/j.envres.2024.118822. Epub 2024 Mar 31.

Joint effects of prenatal exposure to indoor air pollution and psychosocial factors on early life inflammation

Affiliations

Joint effects of prenatal exposure to indoor air pollution and psychosocial factors on early life inflammation

Grace M Christensen et al. Environ Res. .

Abstract

It is hypothesized that air pollution and stress impact the central nervous system through neuroinflammatory pathways Despite this, the association between prenatal exposure to indoor air pollution and psychosocial factors on inflammatory markers in infancy has been underexplored in epidemiology studies. This study investigates the individual and joint effects of prenatal exposure to indoor air pollution and psychosocial factors on early life inflammation (interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α)). We analyzed data from the South African Drakenstein Child Health Study (N = 225). Indoor air pollution and psychosocial factor measurements were taken in the 2nd trimester of pregnancy. Circulating inflammatory markers (IL-1β, Il-6, and TNF-α) were measured in serum in the infants at 6 weeks postnatal. Linear regression models were used to investigate associations between individual exposures and inflammatory markers. To investigate joint effects of environmental and psychosocial factors, Self-Organizing Maps (SOM) were used to create exposure profile clusters. These clusters were added to linear regression models to investigate the associations between exposure profiles and inflammatory markers. All models were adjusted for maternal age, maternal HIV status, and ancestry to control for confounding. Most indoor air pollutants were positively associated with inflammatory markers, particularly benzene and TNF-α in single pollutant models. No consistent patterns were found for psychosocial factors in single-exposure linear regression models. In joint effects analyses, the SOM profile with high indoor air pollution, low SES, and high maternal depressive symptoms were associated with higher inflammation. Indoor air pollutants were consistently associated with increased inflammation in both individual and joint effects models, particularly in combination with low SES and maternal depressive symptoms. The trend for individual psychosocial factors was not as clear, with mainly null associations. As we have observed pro- and anti-inflammatory effects, future research should investigate joint effects of these exposures on inflammation and their health effects.

Keywords: Air pollution; Inflammatory markers; Neuroinflammation; Psychosocial factors.

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Conflict of interest statement

Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Dan Stein reports a relationship with Discovery Vitality that includes: consulting or advisory. Dan Stein reports a relationship with Johnson & Johnson that includes: consulting or advisory. Dan Stein reports a relationship with Kanna that includes: consulting or advisory. Dan Stein reports a relationship with L'Oreal that includes: consulting or advisory. Dan Stein reports a relationship with Orion that includes: consulting or advisory. Dan Stein reports a relationship with Sanofi that includes: consulting or advisory. Dan Stein reports a relationship with Servier that includes: consulting or advisory. Dan Stein reports a relationship with Takeda that includes: consulting or advisory. Dan Stein reports a relationship with Vistagen that includes: consulting or advisory. The other authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Figures

Fig. 1
Fig. 1
Single-exposure linear regression models of the association between prenatal indoor air pollution and psychosocial factor exposures on inflammatory markers at 6 weeks postnatal. All linear regression models were adjusted for maternal age, maternal HIV status, ancestry and socioeconomic status (when not the exposure of interest). A. Models using Il-1β as the outcome. B. Models using Il-6 as the outcome. C. Models using TNF-α as the outcome. Abbreviations: Particulate Matter (PM10); Carbon monoxide (CO); Nitrogen dioxide (NO2); Sulfur dioxide (SO2); Socioeconomic Status (SES); Self-Reporting Questionnaire (SRQ-20); Edinburgh Postnatal Depression Scale (EPDS); Life Experiences Questionnaire (LEQ); Intimate Partner Violence (IPV); Alcohol, Smoking, and Substance Involvement Screening Test (ASSIST); Interleukin 1β (IL-1β); Interleukin 6 (IL-6); Tumor Necrosis Factor-α (TNF-α).
Fig. 2
Fig. 2
Results from self-organizing map (SOM) analysis using prenatal indoor air pollutants and psychosocial factors. A. SOM clusters created using pre-natal indoor air pollutants and psychosocial factors. B. Associations between SOM clusters and IL-1β, adjusted by maternal age, maternal HIV status, and ancestry. SOM cluster 1 is used as the reference group. C. Associations between SOM clusters and IL-6, adjusted by maternal age, maternal HIV status, and ancestry. SOM cluster 1 is used as the reference group. D. Associations between SOM clusters and TNF-α, adjusted by maternal age, maternal HIV status, and ancestry. SOM cluster 1 is used as the reference group. Abbreviations: Particulate Matter (PM10); Carbon monoxide (CO); Nitrogen dioxide (NO2); Sulfur dioxide (SO2); Socioeconomic Status (SES); Self-Reporting Questionnaire (SRQ-20); Edinburgh Postnatal Depression Scale (EPDS); Life Experiences Questionnaire (LEQ); Intimate Partner Violence (IPV); Alcohol, Smoking, and Substance Involvement Screening Test (ASSIST); Interleukin 1β (IL-1β); Interleukin 6 (IL-6); Tumor Necrosis Factor-α (TNF-α).

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