oxic mechanisms of cigarette smoke and heat-not-burn tobacco vapor inhalation on rheumatoid arthriti

Author(s)

Heluany, Cintia Scucuglia ^[1] ; Scharf, Pablo ^[1] ; Schneider, Ayda Henriques ^[2] ; Donate, Paula Barbim ^[2] ; Pedreira Filho, Walter Dos Reis ^[3] ; de Oliveira, Tiago Franco ^[4] ; Cunha, Fernando Queiroz ^[2] ; Poliselli Farsky, Sandra Helena ^[1]

Affiliation

^[1] Univ Sao Paulo, Sch Pharmaceut Sci, Dept Clin & Toxicol Anal, Av Prof Lineu Prestes 580 BL13 B, BR-05508900 Sao Paulo, SP - Brazil

^[2] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Pharmacol, Sao Paulo - Brazil

^[3] Jorge Duprat Figueiredo Fdn Occupat Safety & Med, Minist Econ, Sao Paulo, SP - Brazil

^[4] Fed Univ Hlth Sci Porto Alegre, Dept Pharmacosci, Porto Alegre, RS - Brazil

• Document type: Journal article
• Source: Science of The Total Environment; v. 809, FEB 25 2022.
• Web of Science Citations: 0

Abstract

Tobacco combustion exposure worsens rheumatoid arthritis (RA). Non-combustible tobacco devices, as heat-not-burn tobacco (HNBT), are emerging as harm reduction to smokers by releasing nicotine and lower combustible tobacco products. Nevertheless, HNBT toxicity remains unclear. Hence, here we investigated the impacts of the tobacco combustible product (cigarette smoke; CS) or HNBT vapor exposures on antigen-induced arthritis (AIA) in C57BL/6 mice. Animals were exposed to airflow, HNBT vapor, or CS during 1 h/twice a day, under the Health Canada Intense (HCI) smoking regime, between days 14 to 20 after the first immunization. At day 21, 16 h after the last exposures, mice were i.a. challenged and the AIA effects were evaluated 24 h later. CS- or HNBT-exposed mice presented equivalent blood nicotine levels. CS exposure worsened articular symptoms, pulmonary inflammation, and expression of lung metallothioneins. Nevertheless, CS or HNBT exposures reduced lymphoid organs' cellularity, splenocyte proliferation and IL-2 secretion. Additional in vitro CS or HNBT exposures confirmed the harmful effects on splenocytes, which were partially mediated by the activation of nicotine/alpha 7nAchR pathway. Associated, data demonstrate the toxic mechanisms of CS or HNBT inhalation at HCI regime on RA, and highlight that further investigations are fundamental to assure the toxicity of emerging tobacco products on the immune system during specific challenges. (C) 2021 Elsevier B.V. All rights reserved. (AU)

• FAPESP's process: 19/19573-7 - Effects of the hot not burn tobacco exposure on Rheumatoid Arthritis
• Grantee: Sandra Helena Poliselli Farsky
• Support Opportunities: Regular Research Grants
• FAPESP's process: 13/08216-2 - CRID - Center for Research in Inflammatory Diseases
• Grantee: Fernando de Queiroz Cunha
• Support Opportunities: Research Grants - Research, Innovation and Dissemination Centers - RIDC
• FAPESP's process: 17/26998-9 - Smoking and articular diseases: investigation of hydroquinone and tobacco tube (heatstick) aerosol toxic mechanisms in Rheumatoid Arthritis and Osteoarthritis
• Grantee: Cintia Scucuglia Heluany
• Support Opportunities: Scholarships in Brazil - Post-Doctoral