Search

Background: Chronic obstructive pulmonary disease (COPD) is a preventable, progressive disease and the third leading cause of death worldwide. The epidemiological data of COPD from Gulf countries are very limited, as it remains underdiagnosed and underestimated. Risk factors for COPD include tobacco cigarette smoking, water pipe smoking (Shisha), exposure to air pollutants, occupational dusts, fumes, and chemicals. Inadequate treatment of COPD leads to worsening of disease. The 2024 GOLD guidelines recommend use of inhaled bronchodilators, corticosteroids, and adjunct therapies for treatment and management of COPD patients based on an individual assessment of the severity of symptoms and risk of exacerbations. This article reviews COPD pharmacotherapy in the Gulf countries and explores the role of nebulization in the management of COPD in this region. Methods: To review the COPD pharmacotherapy in the Gulf Countries, literature search was conducted using PubMed, Medline, Cochrane Systematic Reviews, and Google Scholar databases (before December 2022), using search terms such as COPD, nebulization, inhalers/inhalation, aerosols, and Gulf countries. Relevant articles from the reference list of identified studies were reviewed. Consensus statements, expert opinion, and other published review articles were included. Results: In the Gulf countries, pressurized metered-dose inhalers (pMDIs), dry powder inhalers (DPIs), soft mist inhalers, and nebulizers are used for drug delivery to COPD patients. pMDIs and DPIs are most prone to errors in technique and other common device handling errors. Nebulization is another mode of inhalation drug delivery, which is beneficial in certain patient populations such as the elderly and patients with cognitive impairment, motor or neuromuscular disorders, and other comorbidities. Conclusion: There is no major difference between Gulf countries and rest of the world in the approach to management of COPD. Nebulizers should be considered for patients who have difficulties in accessing or using MDIs and DPIs, irrespective of geographical location. [ABSTRACT FROM AUTHOR]

Fine particulate matter (PM2.5) contains carcinogens similar to those generated by tobacco smoking, which may increase the risks of developing smoking‐related cancers, such as upper aerodigestive track (UADT) cancers, for both smokers and never‐smokers. Therefore, it is imperative to understand the relation between ambient PM2.5 exposure and risk of UADT cancers. A population‐based case–control study involving 565 incident UADT cancer cases and 983 controls was conducted in Los Angeles County from 1999 to 2004. The average residential PM2.5 concentration 1 year before the diagnosis date for cases and the reference date for controls was assessed using a chemical transport model. The association between ambient PM2.5 and the UADT cancers was estimated by unconditional logistic regression, adjusting for confounders at the individual and block‐group level. Stratified analyses were conducted by sex, tobacco smoking status and UADT subsites. We also assessed the interaction between PM2.5 and tobacco smoking on UADT cancers. PM2.5 concentrations were associated with an elevated odds of UADT cancers (adjusted odds ratio = 1.21 per interquartile range [4.5 μg/m3] increase; 95% confidence interval: 1.02, 1.44). The association between PM2.5 and UADT cancers was similar across UADT subsites, sex and tobacco smoking status. The interaction between PM2.5 and tobacco smoking on UADT cancers was approximately additive on the odds scale. The effect estimate for PM2.5 and UADT cancers was similar among never smokers. Our findings support the hypothesis that exposure to PM2.5 increases the risk of UADT cancers. Improvements in air quality may reduce the risk of UADT cancers. [ABSTRACT FROM AUTHOR]

Rationale: The slope of FEV 1 decline is commonly used to reflect the rate of disease progression for descriptive studies and therapeutic trials in COPD. Frequency and duration of spirometric testing needed to report the true slope is unknown., Objective: To define the minimum frequency and follow-up duration needed to accurately describe the annualized rate of FEV 1 change among patients with moderate-to-very severe COPD., Methods: We performed a post-hoc analysis of the annualized rate of FEV 1 change among 4412 subjects previously enrolled in the four-year UPLIFT trial of tiotropium versus placebo. Slope estimates were modeled for different iterations of semiannual or annual testing over a variable duration up to four years. All models were compared to a reference of semiannual spirometry for four years., Measurements and Main Results: The overall rate of post-bronchodilator FEV 1 decline measured semi-annually for four years (44.6 ml; 95% CI:42.5-46.6) did not differ significantly from annual spirometry over the same period (43.7 ml; 95% CI:41.3-46.1) or semiannual spirometry over the first two years (44.3 ml; 95% CI:41.1-47.5). Agreement was consistent for two follow-up values as far as 24 months apart (43.3ml; 95% CI:39.9-46.8). Models based on less than two follow-up values or duration less than 18 months were characterized by relative underestimation of the slope., Conclusions: In a large cohort of patients with moderate-to-very severe COPD, the annualized rate of change in FEV 1 was accurately represented by a minimum of two follow-up measurements over 18 months compared to semiannual testing over four years.

The widespread use of marijuana in the context of increasing legalization has both short- and long-term health implications. Although various modes of marijuana use-smoked, vaped, or ingested-may lead to a wide scope of potential systemic effects, we focus here on inhalational use of marijuana as the most common mode with the lung as the organ that is most directly exposed to its effects. Smoked marijuana has been associated with symptoms of chronic bronchitis and histopathologic changes in airway epithelium, but without consistent evidence of long-term decline in pulmonary function. Its role in immunomodulation, both for risk of infection and protection against a hyperinflammatory host response to infection, has been suggested in animal models and in vitro without conclusive extrapolation to humans. Marijuana smoke contains carcinogens like those found in tobacco, raising concern about its role in lung cancer, but evidence is mixed and made challenging by concurrent tobacco use. Vaping may offer a potential degree of harm reduction when compared with smoking marijuana with reduction of exposure to several toxins, including carbon monoxide, and reduction in chronic respiratory symptoms. However, these potential benefits are counterbalanced by risks including vaping-associated lung injury, potentially more intense drug exposure, and other yet not well-understood toxicities. As more states legalize marijuana and the federal government considers changing this from a Schedule I to a Schedule III controlled substance, we anticipate an increase in prospective medical studies concerning the risks related to marijuana use. This review is based on currently available data concerning the impact of inhaled marijuana on lung health., Competing Interests: Disclosure The authors report no conflicts of interest in this work., (Thieme. All rights reserved.)

Fine particulate matter (PM 2.5 ) contains carcinogens similar to those generated by tobacco smoking, which may increase the risks of developing smoking-related cancers, such as upper aerodigestive track (UADT) cancers, for both smokers and never-smokers. Therefore, it is imperative to understand the relation between ambient PM 2.5 exposure and risk of UADT cancers. A population-based case-control study involving 565 incident UADT cancer cases and 983 controls was conducted in Los Angeles County from 1999 to 2004. The average residential PM 2.5 concentration 1 year before the diagnosis date for cases and the reference date for controls was assessed using a chemical transport model. The association between ambient PM 2.5 and the UADT cancers was estimated by unconditional logistic regression, adjusting for confounders at the individual and block-group level. Stratified analyses were conducted by sex, tobacco smoking status and UADT subsites. We also assessed the interaction between PM 2.5 and tobacco smoking on UADT cancers. PM 2.5 concentrations were associated with an elevated odds of UADT cancers (adjusted odds ratio = 1.21 per interquartile range [4.5 μg/m 3 ] increase; 95% confidence interval: 1.02, 1.44). The association between PM 2.5 and UADT cancers was similar across UADT subsites, sex and tobacco smoking status. The interaction between PM 2.5 and tobacco smoking on UADT cancers was approximately additive on the odds scale. The effect estimate for PM 2.5 and UADT cancers was similar among never smokers. Our findings support the hypothesis that exposure to PM 2.5 increases the risk of UADT cancers. Improvements in air quality may reduce the risk of UADT cancers., (© 2024 The Authors. International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC.)