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For decades, many studies have linked maternal smoking to an increased risk of preterm birth. As a result, the scientific community has long hypothesized that exposure to environmental tobacco smoke (ETS), commonly referred to as second-hand smoke, is also associated with an increased risk of preterm birth. Multiple studies have examined this proposed association through different strategies and approaches. Recently, a small number of epidemiology studies have examined preterm birth trends before and after the implementation of antismoking legislation in various jurisdictions. We found that these studies have largely revealed a significant trend of decreasing population-level preterm birth rates after the implementation of smoking bans. However, most of the studies reviewed did not distinguish the impact of maternal smoking from ETS in their analyses, making it difficult to specifically evaluate the effects of smoking bans on ETS exposure. Other studies have taken the approach of directly measuring maternal ETS exposure and associations with preterm birth within particular study populations. In contrast to smoking ban studies, the latter group of studies had more inconclusive results. The use of a variety of exposure assessment methods ranging from different self-reporting techniques to biomarker measurements posed a challenge to compare studies. We evaluate current scientific literature for evidence of an association between maternal ETS exposure and risk of preterm birth. We also discuss the strengths and weaknesses of the different approaches to study this association as well as methods used for ETS exposure assessment. We propose that more studies, specifically, evaluating rates of preterm birth among nonsmoking women before and after smoking bans, are needed as well as using better ETS exposure assessments methods in studies measuring maternal ETS exposure.
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http://dx.doi.org/10.1021/acs.chemrestox.7b00054 | DOI Listing |
Nutrients
August 2025
Department of Biological, Chemical and Pharmaceutical Sciences and Technologies (STeBiCeF), University of Palermo, Viale delle Scienze, Building 16, 90128 Palermo, Italy.
: Nutrigenomics explores how dietary components influence genome function, especially via epigenetic mechanisms like DNA methylation. A key challenge is identifying healthy food-derived molecules capable of counteracting epigenetic damage from harmful dietary elements. Pistachio nuts ( L.
View Article and Find Full Text PDFFront Toxicol
August 2025
Reemtsma Cigarettenfabriken GmbH, An Imperial Brands PLC company, Hamburg, Germany.
Data from pre-clinical and clinical studies form part of an integrated assessment of the tobacco harm reduction (THR) potential of novel products that may act as cigarette alternatives for adult smokers. We report data from pre-clinical (emissions chemistry and toxicology) and clinical (nicotine pharmacokinetics and subjective effects) studies conducted with the iSENZIA™ heated herbal system (HHS; PULZE™ 2.0 device with iSENZIA™ sticks), which utilizes electronic heating of a tea-based substrate to generate an inhalable nicotine-containing aerosol.
View Article and Find Full Text PDFCancer Epidemiol
August 2025
University of California, San Diego, School of Medicine, San Diego, CA, USA. Electronic address:
Background: Environmental tobacco smoke (ETS), also known as passive smoke, is a major public health concern due to its adverse health effects, which are comparable to those of active smoking. Although the risks of ETS for cardiovascular and respiratory outcomes are well documented, less is known about its impact on cancer prognosis. This study evaluated the association between ETS exposure and five-year all-cause mortality among patients diagnosed with breast, colorectal, lung, melanoma, or stomach cancer.
View Article and Find Full Text PDFAdv Sci (Weinh)
August 2025
Department of Neurology, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, 710004, China.
Ischemia reperfusion (I/R) injury associated with recanalization therapy in acute ischemic stroke (AIS) exacerbates the initial brain damage. However, it remains a clinical challenge due to limited understanding of the underlying mechanisms of I/R injury. This study aims to investigate the mechanism of succinate dehydrogenase (SDH)-mediated succinate oxidation in microglia extracellular traps (MiETs) formation and neuronal injury after cerebra I/R injury.
View Article and Find Full Text PDFbioRxiv
August 2025
Department of Otolaryngology, University of Pittsburgh, Pittsburgh, PA.
Peripheral trauma, such as noise-induced hearing loss (NIHL), triggers compensatory plasticity in the auditory cortex (ACtx) to maintain auditory function. While cortical plasticity in superficial cortical layers has been relatively well studied, the plasticity mechanisms governing deep-layer excitatory projection neurons remain less understood. Here, we investigated the plasticity of layer (L)5 extratelencephalic (ETs) and L6 corticothalamic neurons (CTs) following NIHL.
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