Toxic mechanisms of cigarette smoke and heat-not-burn tobacco vapor inhalation on rheumatoid arthritis

Heluany, Cíntia Scucuglia; Scharf, Pablo; Schneider, Ayda Henriques; Donate, Paula B.; Filho, Walter dos Reis Pedreira; Oliveira, Tiago Franco de; Cunha, Fernando Q.; Farsky, Sandra Helena Poliselli

doi:10.1016/j.scitotenv.2021.151097

Cited by 12 publications

(12 citation statements)

References 64 publications

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“…For instance, Donate et al demonstrated that smoking can activate the aryl hydrocarbon receptor on Th17 cells in RA patients, thereby upregulating miR-132 and inhibiting the induction of cyclooxygenase-2, resulting in worsened arthritis inflammation and bone destruction ( 32 ). Recent toxic mechanism study conducted by Heluany et al has also demonstrated that smoking can exacerbate joint symptoms, lung inflammation and lung metallothionein expression, and cause toxic damage to splenocytes by activating the nicotine/α7 nicotinic acetylcholine receptor pathway ( 33 ). Regarding physical exercise, many randomized trials have emphasized its benefits for RA patients’ pain and disability ( 34 ).…”

Section: Discussionmentioning

confidence: 99%

Association between Life’s simple 7 and rheumatoid arthritis in adult Americans: data from the National Health and nutrition examination survey

Wang,

Xing,

Sheng

et al. 2023

Front. Public Health

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ObjectiveThe study aimed to investigate the relationship between Life’s Simple 7 (LS7) and the risk of rheumatoid arthritis (RA) in adult Americans.MethodsA total of 17,532 participants were included in this study. The association between LS7 and the risk of RA was assessed using a weighted logistic regression model, with odds ratios (ORs) and 95% confidence intervals (CIs) calculated. Moreover, the nonlinear relationship was further characterized through smooth curve fitting (SCF) and weighted generalized additive model (GAM) analysis.ResultsAfter adjusting for all covariates, the weighted logistic regression model demonstrated that the LS7 was negatively correlated with the risk of RA. Compared to quintile 1 of LS7, the OR between the risk of RA and quartile 4 of LS7 (LS7.Q4) was 0.261 (95% CI, 0.203, 0.337) in males under 50 years old, while in females of the same age group, the OR was 0.183 (95% CI, 0.142, 0.234). For females aged between 50 and 70 years old, the OR between the risk of RA and LS7.Q4 was 0.313 (95% CI, 0.264, 0.371). In females aged 70 years or older, the OR between the risk of RA and LS7.Q4 was 0.632 (95% CI, 0.486, 0.822).ConclusionThis finding suggested the healthy lifestyle behaviors represented by LS7 have a negative association with RA. However, further prospective studies are needed to verify the causal relationship in the results.

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Section: Discussionmentioning

confidence: 99%

Association between Life’s simple 7 and rheumatoid arthritis in adult Americans: data from the National Health and nutrition examination survey

Wang,

Xing,

Sheng

et al. 2023

Front. Public Health

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“…CeD is associated with several autoimmune diseases and asthma (Krishna et al, 2019), and numerous studies have shown that cigarette exposure is associated with the development of allergies and asthma (Murrison et al, 2019). Studies have also shown that cigarette smoke is a risk factor for RA (Heluany et al, 2021), IBD (van der Sloot et al, 2020), and colorectal tumors (van der Sloot et al, 2022). A meta-analysis of seven studies with 307,924 participants suggested that current smokers presented a markedly decreased risk of CeD compared with never-smokers (Wijarnpreecha et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Identifying celiac disease-related chemicals by transcriptome-wide association study and chemical-gene interaction analyses

Feng

Liu

et al. 2022

Front. Genet.

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Celiac disease (CeD) is one of the most common intestinal inflammatory diseases, and its incidence and prevalence have increased over time. CeD affects multiple organs and systems in the body, and environmental factors play a key role in its complex pathogenesis. Although gluten exposure is known to be the causative agent, many unknown environmental factors can trigger or exacerbate CeD. In this study, we investigated the influence of genetic and environmental factors on CeD. Data from a CeD genome-wide association study that included 12,041 CeD cases and 12,228 controls were used to conduct a transcriptome-wide association study (TWAS) using FUSION software. Gene expression reference data were obtained for the small intestine, whole blood, peripheral blood, and lymphocytes. We performed Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses using the significant genes identified by the TWAS and conducted a protein–protein interaction network analysis based on the STRING database to detect the function of TWAS-identified genes for CeD. We also performed a chemical-related gene set enrichment analysis (CGSEA) using the TWAS-identified genes to test the relationships between chemicals and CeD. The TWAS identified 8,692 genes, including 101 significant genes (padjusted < 0.05). The CGSEA identified 2,559 chemicals, including 178 chemicals that were significantly correlated with CeD. This study performed a TWAS (for genetic factors) and CGSEA (for environmental factors) and identified several CeD-associated genes and chemicals. The findings expand our understanding of the genetic and environmental factors related to immune-mediated diseases.

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“…With respect to the articles identified that described in vitro toxicological analyses of HTPs, articles were excluded from detailed discussion in this section of the review if they did not detail a direct quantitative comparison between the HTP(s) under investigation and other nicotine-or tobacco-containing products such as cigarettes and/or EVPs (i.e., statistical analyses were reported solely between the effects of the HTP and the negative control used) [64,65]; investigated any cell line not related to tissues of the oral cavity, respiratory tract, cardiovascular system or pluripotent stem cells [66][67][68][69][70][71][72]; attempted to investigate different human exposure scenarios using the same experimental methodology (i.e., sidestream smoke released by cigarettes being compared to aerosol produced by an HTP as a means of comparing bystander exposure between products) [67].…”

Section: In Vitro Toxicologymentioning

confidence: 99%

“…A total of twelve articles were identified that detailed an in vivo assessment of the effects of exposure to HTPs [66,70,[96][97][98][99][100][101][102][103][104][105]. Eleven articles provided novel data [66,70,96,[98][99][100][101][102][103][104][105] while one study provided a secondary analysis of data from a previous study [97]. All identified studies investigated the in vivo effects of exposure to HTPs in either mice or rats.…”

Section: In Vivo Toxicologymentioning

confidence: 99%

The Product Science of Electrically Heated Tobacco Products: An Updated Narrative Review of the Scientific Literature

Cordery,

Thompson,

Stevenson

et al. 2024

Cureus

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Heated tobacco products represent a novel category of tobacco products in which a tobacco consumable is heated to a temperature that releases nicotine from the tobacco leaf but not to a temperature sufficient to cause combustion. Heated tobacco products may therefore have the potential to be a less harmful alternative for adult smokers who would otherwise continue to smoke cigarettes, as their use should result in exposure to substantially fewer and lower levels of toxicants. This update represents a two-year extension to our previous narrative review, which covered peer-reviewed journal articles published up to August 31, 2021. The scientific evidence published between 2021 and 2023 continues to indicate that aerosols produced from heated tobacco products contain fewer and substantially lower levels of harmful and potentially harmful constituents and that these observed reductions consistently translate to reduced biological effects in both in vitro and in vivo toxicological studies. Biomarker and clinical data from studies in which product use is controlled within a clinical setting continue to suggest changes in levels of biomarkers of exposure, biomarkers of potential harm, and clinical endpoints indicating the potential for reduced harm with switching to exclusive use of heated tobacco products in adult smokers. Overall, the available peer-reviewed scientific evidence continues to indicate that heated tobacco products offer promise as a potentially less harmful alternative to cigarettes, and as such, the conclusions of our original narrative review remain valid.

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Toxic mechanisms of cigarette smoke and heat-not-burn tobacco vapor inhalation on rheumatoid arthritis

Cited by 12 publications

References 64 publications

Association between Life’s simple 7 and rheumatoid arthritis in adult Americans: data from the National Health and nutrition examination survey

Association between Life’s simple 7 and rheumatoid arthritis in adult Americans: data from the National Health and nutrition examination survey

Identifying celiac disease-related chemicals by transcriptome-wide association study and chemical-gene interaction analyses

The Product Science of Electrically Heated Tobacco Products: An Updated Narrative Review of the Scientific Literature

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