Secondhand smoke exposure and serum cytokine levels in healthy children

Wilson, Karen M.; Wesgate, Sarah C.; Pier, Jennifer; Weis, Emily; Love, Tanzy; Evans, K.; Chhibber, Ashwani K.

doi:10.1016/j.cyto.2012.06.236

Cited by 15 publications

(14 citation statements)

References 20 publications

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“…Our study showed an insignificant association between maternal SHS exposure during pregnancy and maternal serum CRP levels. Regarding the associations between SHS exposure and three pro-inflammatory markers, IL-1β, IL-6 and TNF-α, Wilson et al found that healthy children exposed to SHS had lower serum concentrations of IL-1β than those without SHS exposure 23 , but an inverse association was observed in adults 24 and an insignificant association in adolescents was reported by Matsunaga et al 22 . Five studies found that SHS exposure had no significant effect on serum IL-6 in adolescents 22 23 and adults 9 21 24 , while a study in the elderly reported a significant association between SHS and elevated serum IL-6 levels 25 .…”

Section: Discussionmentioning

confidence: 97%

“…Regarding the associations between SHS exposure and three pro-inflammatory markers, IL-1β, IL-6 and TNF-α, Wilson et al found that healthy children exposed to SHS had lower serum concentrations of IL-1β than those without SHS exposure 23 , but an inverse association was observed in adults 24 and an insignificant association in adolescents was reported by Matsunaga et al 22 . Five studies found that SHS exposure had no significant effect on serum IL-6 in adolescents 22 23 and adults 9 21 24 , while a study in the elderly reported a significant association between SHS and elevated serum IL-6 levels 25 . An insignificant association between SHS exposure and serum TNF-α was reported by four studies, two in adolescents 22 23 and two in adults 9 24 , and a positive association was reported by another study in adults 24 .…”

Section: Discussionmentioning

confidence: 97%

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Potential pathways by which maternal second-hand smoke exposure during pregnancy causes full-term low birth weight

Niu

Xie

Wen

et al. 2016

Sci Rep

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It is well documented that maternal exposure to second-hand smoke (SHS) during pregnancy causes low birth weight (LBW), but its mechanism remains unknown. This study explored the potential pathways. We enrolled 195 pregnant women who delivered full-term LBW newborns, and 195 who delivered full-term normal birth weight newborns as the controls. After controlling for maternal age, education level, family income, pre-pregnant body mass index, newborn gender and gestational age, logistic regression analysis revealed that LBW was significantly and positively associated with maternal exposure to SHS during pregnancy, lower placental weight, TNF-α and IL-1β, and that SHS exposure was significantly associated with lower placental weight, TNF-α and IL-1β. Structural equation modelling identified two plausible pathways by which maternal exposure to SHS during pregnancy might cause LBW. First, SHS exposure induced the elevation of TNF-α, which might directly increase the risk of LBW by transmission across the placenta. Second, SHS exposure first increased maternal secretion of IL-1β and TNF-α, which then triggered the secretion of VCAM-1; both TNF-α and VCAM-1 were significantly associated with lower placental weight, thus increasing the risk of LBW. In conclusion, maternal exposure to SHS during pregnancy may lead to LBW through the potential pathways of maternal inflammation and lower placental weight.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 97%

Potential pathways by which maternal second-hand smoke exposure during pregnancy causes full-term low birth weight

Niu

Xie

Wen

et al. 2016

Sci Rep

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“…Wilson et al [ 142 ] reported that exposure of children to secondhand smoke produced significant changes in cytokine levels particularly reducing the level of IFN- γ . As previously mentioned in the section on Pb, Lutz et al [ 137 ] reported an interaction of environmental risk factors in which Pb-exposed children also exposed to ETS had elevated IgE and IL-4 levels and altered T cell populations.…”

Section: Human Studies Involving Dit: Alphabetical List Of Risk Famentioning

confidence: 99%

Developmental Immunotoxicity, Perinatal Programming, and Noncommunicable Diseases: Focus on Human Studies

Dietert

2014

Advances in Medicine

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Developmental immunotoxicity (DIT) is a term given to encompass the environmentally induced disruption of normal immune development resulting in adverse outcomes. A myriad of chemical, physical, and psychological factors can all contribute to DIT. As a core component of the developmental origins of adult disease, DIT is interlinked with three important concepts surrounding health risks across a lifetime: (1) the Barker Hypothesis, which connects prenatal development to later-life diseases, (2) the hygiene hypothesis, which connects newborns and infants to risk of later-life diseases and, (3) fetal programming and epigenetic alterations, which may exert effects both in later life and across future generations. This review of DIT considers: (1) the history and context of DIT research, (2) the fundamental features of DIT, (3) the emerging role of DIT in risk of noncommunicable diseases (NCDs) and (4) the range of risk factors that have been investigated through human research. The emphasis on the human DIT-related literature is significant since most prior reviews of DIT have largely focused on animal research and considerations of specific categories of risk factors (e.g., heavy metals). Risk factors considered in this review include air pollution, aluminum, antibiotics, arsenic, bisphenol A, ethanol, lead (Pb), maternal smoking and environmental tobacco smoke, paracetamol (acetaminophen), pesticides, polychlorinated biphenyls, and polyfluorinated compounds.

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“…14 Additionally, there is evidence that secondhand smoke exposure in children is related to differing levels of inflammatory cytokines. 15 In this study, we examined the association between cytokine levels in children with bronchiolitis and an asthma visit 6 months after discharge. We hypothesized that children with elevated Th2 cytokines (IL-4, IL-6 and IL-13) would be more likely to have a follow-up asthma visit compared with those with normal levels and that tobacco and marijuana smoke exposure would be associated with cytokine levels and asthma follow-up visits.…”

mentioning

confidence: 99%

Smoke Exposure, Cytokine Levels, and Asthma Visits in Children Hospitalized for Bronchiolitis

Willis¹,

Moss²,

Torok³

et al. 2019

Hospital Pediatrics

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A B S T R A C T BACKGROUND AND OBJECTIVE:To determine if cigarette smoke exposure, marijuana smoke exposure, or cytokine levels at admission to the hospital for bronchiolitis are associated with follow-up visits for asthma. METHODS:We enrolled a cohort of children aged 31 days to 2 years who were hospitalized with bronchiolitis from January 2013 to April 2014. Data included the results of a baseline survey about children's health and demographics, nasal wash samples, the results of a 6-month postdischarge follow-up survey, and a chart review. Nasal wash samples were tested for interleukin (IL)-6, IL-13, and tumor necrosis factor a (TNF-a); values were categorized for analysis. x 2 , Fisher's exact, and Wilcoxon rank tests were done to test bivariable differences; all analyses were done using SAS. RESULTS:We approached 180 families for enrollment; 99 consented to participate, and 74% of these completed follow-up surveys. Half of those with high levels of IL-13 had follow-up visits for asthma, whereas only 4.2% of those with low levels had follow-up visits for asthma (P 5 .02). Marijuana exposure was reported for 12.5% (n 5 7) of study participants. There was a significant association between marijuana exposure and TNF-a levels (P 5 .03). CONCLUSIONS:Our study revealed an association between IL-13 and follow-up visits for asthma in children who were hospitalized with bronchiolitis. We found an association between family-reported marijuana smoke exposure and detectable but lower levels of TNF-a. Further research is needed to study these relationships.

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Secondhand smoke exposure and serum cytokine levels in healthy children

Cited by 15 publications

References 20 publications

Potential pathways by which maternal second-hand smoke exposure during pregnancy causes full-term low birth weight

Potential pathways by which maternal second-hand smoke exposure during pregnancy causes full-term low birth weight

Developmental Immunotoxicity, Perinatal Programming, and Noncommunicable Diseases: Focus on Human Studies

Smoke Exposure, Cytokine Levels, and Asthma Visits in Children Hospitalized for Bronchiolitis

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