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E-cigarette or vaping product use-associated lung injury (EVALI) is a severe pulmonary illness associated with the use of e-cigarettes or vaping products that was officially identified and named in 2019. This American Thoracic Society workshop was convened in 2021 to identify and prioritize research and regulatory needs to adequately respond to the EVALI outbreak and to prevent similar instances of disease associated with e-cigarette or vaping product use. An interdisciplinary group of 26 experts in adult and pediatric clinical care, public health, regulatory oversight, and toxicology were convened for the workshop. Four major topics were examined: 1) the public health and regulatory response to EVALI; 2) EVALI clinical care; 3) mechanisms contributing to EVALI; and 4) needed actions to address the health effects of EVALI. Oral presentations and group discussion were the primary modes used to identify top priorities for addressing EVALI. Initiatives including a national EVALI case registry and biorepository, integrated electronic medical record coding system, U.S. Food and Drug Administration regulation and enforcement of nicotine e-cigarette standards, regulatory authority over nontobacco-derived e-cigarettes, training in evaluating exogenous exposures, prospective clinical studies, standardized clinical follow-up assessments, ability to more readily study effects of cannabinoid e-cigarettes, and research to identify biomarkers of exposure and disease were identified as critical needs. These initiatives will require substantial federal investment as well as changes to regulatory policy. Overall, the workshop identified the need to address the root causes of EVALI to prevent future outbreaks. An integrated approach from multiple perspectives is required, including public health; clinical, basic, and translational research; regulators; and users of e-cigarettes. Improving the public health response to reduce the risk of another substantial disease-inducing event depends on coordinated actions to better understand the inhalational toxicity of these products, informing the public of the risks, and developing and enforcing regulatory standards for all e-cigarettes.

To date, while the FDA mandates reporting added sugar levels on packaged foods and beverages "to make it easier for you to make informed choices",[20] this mandate does not extend to tobacco and nicotine products. Under current federal regulations, tobacco and vaping manufacturers are not required to disclose sugar and sweetener levels on their product packaging or marketing materials (Figure 1). For the 5th National Institute of Health Tobacco Regulatory Science meeting, we participated in a plenary session focused on sugars and sweeteners profiles in tobacco and nicotine products and their related toxicity and abuse liability implications. [Extracted from the article]

BACKGROUND: Although it is known that acetaminophen causes oxidative injury in the liver, it is not known whether it causes oxidative stress in the respiratory tract. If so, this widely used analgesic may potentiate the adverse effects of oxidant air pollutants. OBJECTIVES: The goal of this study was to determine if acetaminophen induces respiratory tract oxidative stress and/or potentiates the oxidative stress and irritant responses to an inhaled oxidant: environmental tobacco smoke (ETS). METHODS: Acetaminophen [100 mg/kg intraperitoneal (ip)] and/or sidestream tobacco smoke (as a surrogate for ETS, 5 mg/[m.sup.3] for 10 min) were administered to female C57Bl/6J mice, and airway oxidative stress was assessed by loss of tissue antioxidants [estimated by nonprotein sulfhydryl (NPSH) levels] and/or induction of oxidant stress response genes. In addition, the effects of acetaminophen on airway irritation reflex responses to ETS were examined by plethysmography. RESULTS: Acetaminophen diminished NPSH in nasal, thoracic extrapulmonary, and lung tissues; it also induced the oxidant stress response genes glutamate-cysteine ligase, catalytic subunit, and NAD(P)H dehydrogenase, quinone 1, in these sites. ETS produced a similar response. The response to acetaminophen plus ETS was equal to or greater than the sum of the responses to either agent alone. Although it had no effect by itself, acetaminophen greatly increased the reflex irritant response to ETS. CONCLUSIONS: At supratherapeutic levels, acetaminophen induced oxidative stress throughout the respiratory tract and appeared to potentiate some responses to environmentally relevant ETS exposure in female C57Bl/6J mice. These results highlight the potential for this widely used drug to modulate responsiveness to oxidant air pollutants. http://dx.doi.org/10.1289/ehp.1509851, Introduction Oxidative stress results from an imbalance between antioxidants and prooxidants within a cell. Oxidative stress is a common mechanism for respiratory tract injury by inhaled as well as by [...]

Chlorine gas is one of the highly produced chemicals in the USA and around the world. Chlorine gas has several uses in water purification, sanitation, and industrial applications; however, it is a toxic inhalation hazard agent. Inhalation of chlorine gas, based on the concentration and duration of the exposure, causes a spectrum of symptoms, including but not limited to lacrimation, rhinorrhea, bronchospasm, cough, dyspnea, acute lung injury, death, and survivors develop signs of pulmonary fibrosis and reactive airway disease. Despite the use of chlorine gas as a chemical warfare agent since World War I and its known potential as an industrial hazard, there is no specific antidote. The resurgence of the use of chlorine gas as a chemical warfare agent in recent years has brought speculation of its use as weapons of mass destruction. Therefore, developing antidotes for chlorine gas-induced lung injuries remains the need of the hour. While some of the pre-clinical studies have made substantial progress in the understanding of chlorine gas-induced pulmonary pathophysiology and identifying potential medical countermeasure(s), yet none of the drug candidates are approved by the U.S. Food and Drug Administration (FDA). In this review, we summarized pathophysiology of chlorine gas-induced pulmonary injuries, pre-clinical animal models, development of a pipeline of potential medical countermeasures under FDA animal rule, and future directions for the development of antidotes for chlorine gas-induced lung injuries. [ABSTRACT FROM AUTHOR]