Emphysema

Smoking Tobacco Plus Weed Greatly Raises Odds for Emphysema

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News Picture: Smoking Tobacco Plus Weed Greatly Raises Odds for EmphysemaBy Dennis Thompson HealthDay Reporter

TUESDAY, Nov. 28, 2023 (HealthDay News)

Folks who smoke weed along with cigarettes are doing serious damage to their lungs, a new study warns.

People who do both are 12 times more likely to develop emphysema than nonsmokers, due to the damage they’re doing to the lung’s air sacs, researchers report.

“There is a common public misconception that marijuana smoking is not harmful,” said researcher Dr. Jessie Kang, a cardiothoracic radiologist at Dalhousie University in Nova Scotia, Canada.

“With our study, we show that there are physical effects of marijuana smoking on the lungs and that cigarette smoking and marijuana smoking may have a combined damaging effect on the lungs,” Kang added.

Even though weed is one of the most widely used psychoactive substances in the world, little is known about the effects of smoking cannabis on a person’s lung health, researchers noted.

Tons of research has linked cigarette smoking to lung cancer, emphysema and COPD, but “currently not much research exists on the effects of marijuana smoking on the lungs,” Kang noted.

For their study, Kang and her colleagues examined chest CT images of four patient groups – nonsmokers, cigarette smokers, marijuana smokers and combined tobacco and weed smokers.

Weed smokers included in the study had toked at least four times a month for at least two years, researchers said.

In addition to increased risk of emphysema, combined weed and cigarette smokers also were three to four times more likely to have airway wall thickening, researchers said. This thickening can contribute to infections, scarring and further airway damage.

The association with emphysema and airway wall thickening was not as significant for people who smoked either weed or cigarettes alone, results show.

This could mean that weed and cigarette smoke might somehow interact with each other to have even worse effects on the lungs and airways, the researchers said.

The findings were to be presented Tuesday at the Radiological Society of North America (RSNA) meeting in Chicago. Research presented at a medical meeting should be considered preliminary until published in a peer-reviewed journal.

“The [average] number of marijuana smoking years was less than compared to cigarette smokers and combined marijuana and cigarette smokers,” Kang said in a meeting news release. “However, marijuana that is smoked is often unfiltered, which can potentially lead to more damaging particles entering the airways and lungs.”

“More research needs to be done in this area, so the public can make an informed decision on their recreational usage of marijuana,” Kang added.

Nine controversial questions about augmentation therapy for alpha-1 antitrypsin deficiency: a viewpoint

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Abstract

Augmentation therapy with intravenous alpha-1 antitrypsin is the only specific treatment for alpha-1 antitrypsin deficiency (AATD)-associated emphysema. This treatment has been available and remained basically unchanged for more than 35 years, but many questions persist regarding its indications, regimen of administration and efficacy. Because AATD is a rare disease, it has not been possible to conduct randomised, placebo-controlled trials that are adequately powered for the usual outcomes analysed in non-AATD-related COPD, such as lung function decline, exacerbations, symptoms or quality of life. New outcomes such as lung densitometry measured by computed tomography are more sensitive for identifying emphysema progression but are not widely accepted by regulatory agencies. In addition, clinical manifestations, severity and the natural history of lung disease associated with AATD are very heterogeneous, which means that individual prediction of prognosis is challenging. Therefore, the indication for augmentation is sometimes a dilemma between initiating treatment in individuals who may not develop significant lung disease or in whom disease will not progress and delaying it in patients who will otherwise rapidly and irreversibly progress.

Other areas of debate are the possible indication for augmentation in patients with severe AATD and respiratory diseases other than emphysema, such as bronchiectasis or asthma, and the use of therapy after lung transplant in AATD patients. All these uncertainties imply that the indication for treatment must be personalised in expert reference centres after in-depth discussion of the pros and cons of augmentation with the patient.

Conclusions

Although AT has been in use for more than 30 years, there is large variability in its use and there are still several uncertainties regarding its indication. A personalised approach to the indication and treatment regimen seems to be the most adequate, but there is a lack of evidence about aspects, such as the right protective threshold for each patient, the efficacy of different treatment regimens and the right outcome for evaluating the evolution of emphysema. Currently, there is no evidence for the treatment of Pi*MZ or Pi*SZ heterozygotes, or patients with AATD and bronchiectasis or asthma without significant or progressive coexistent emphysema. In this context, individualised prescription in reference centres with a discussion between the patient and the healthcare provider on the pros and cons of AT is necessary.

Air pollution may accelerate emphysema progression

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Long-term exposure to common air pollutants is associated with significant progression of emphysema, according to an 18-year study published in JAMA.

“We were surprised to see how strong air pollution’s impact was on the progression of emphysema on lung scans, in the same league as the effects of cigarette smoking, which is by far the best-known cause of emphysema,” Joel D. Kaufman, MD, MPH, professor of occupational health sciences and epidemiology at the University of Washington School of Public Health and professor of internal medicine at the University of Washington School of Medicine, said in a press release.

For instance, the researchers found that living in an area that had an ambient ozone level that was 3 parts per billion (ppb) higher than another location over 10 years was linked to an increase in emphysema that was comparable to 3 years of aging or to smoking a pack of cigarettes per day for 29 years.

“Rates of chronic lung disease in this country are going up, and increasingly it is recognized that this disease occurs in nonsmokers,” Kaufman said. “We really need to understand what’s causing chronic lung disease, and it appears that air pollution exposures that are common and hard to avoid might be a major contributor.”

Adverse effects

For this study, the researchers evaluated the association between resident-specific concentrations of ozone (O3), fine particulate matter (PM2.5), oxides of nitrogen (NOx) and black carbon, as estimated by spatiotemporal models, with percent emphysema, as assessed by CT imaging or lung function.

The cohort included participants in the Multi-Ethnic Study of Atherosclerosis (MESA) Lung and Air studies conducted in Chicago; Baltimore; Winston-Salem, North Carolina; Los Angeles; St. Paul, Minnesota; and New York. Participants were recruited from 2000 to 2002, with additional participants recruited from 2005 to 2007, and follow-up was available through 2018.

Long-term exposure to common air pollutants is associated with significant progression of emphysema, according to an 18-year study published in JAMA.

Source: Adobe Stock

Of the 7,071 study participants (mean age at recruitment, 60 years; 47.1% men), 5,780 were assigned outdoor residential air pollution concentrations at baseline and during follow-up and had at least one follow-up CT scan during a median of 10 years.

At baseline, median percent emphysema was 3% and increased by a mean 0.58 percentage points per 10 years. Although mean concentrations of PM2.5 and NOx decreased during follow-up, O3 did not.

Overall, results linked greater long-term exposures to air pollutants at baseline and greater exposures to black carbon through 2006 to 2008 to increased progression of emphysema over 10 years. Specifically, percent emphysema increased by 0.13 percentage points per 3 ppb of O3, by 0.11 percentage points per 2 g/m3 of PM2.5, by 0.06 percentage points per 10 ppb of NOx and by 0.1 percentage points per 0.2 g/m3 of black carbon.

Additionally, a 3 ppb-higher long-term O3 exposure was associated with an increased progression of 0.18 percentage points in percent emphysema over 10 years and a 10 ppb-higher long-term NOx exposure was associated with an increased progression of 0.12 percentage points in percent emphysema over 10 years. However, there was no significant association between PM2.5 and faster progression of emphysema.

Furthermore, 3 ppb in long-term O3 exposure during follow-up was associated with an 18.15-mL greater decrease in FEV1 and a 40.19-mL decrease in FVC over 10 years. Other air pollutants, however, did not appear to be linked to declines in lung function.

Concerns over climate change

These findings raise concerns about the effect of the environment on respiratory disease, especially given the growing issue of climate change.

“This is a big study with a state-of-the art analysis of more than 15,000 CT scans repeated on thousands of people over as long as 18 years. These findings matter since ground-level ozone levels are rising, and the amount of emphysema on CT scans predicts hospitalization from and deaths due to chronic lung disease,” study author R. Graham Barr, MD, DrPH, professor medicine and epidemiology at Columbia University, said in the release. “As temperatures rise with climate change, ground-level ozone will continue to increase unless steps are taken to reduce this pollutant. But it’s not clear what level of the air pollutants, if any, is safe for human health.” – by Melissa Foster

A CenturiesOld Chinese Herbal Medicine Could Help Us to Fight TB

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As science struggles to find new chemicals to address old afflictions, one more time an ancient — and wholly natural — remedy may be the answer, in this case with fighting tuberculosis (TB), according to Science Alert. It turns out that a compound called arteminsinin, which comes from a form of wormwood, not only treats malaria, but antibiotic-resistant TB bacteria.

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While the research is ongoing, it adds to the growing body of evidence that Mother Nature more often than not has the solution to common illnesses. Antibiotics are a foundational component of modern medicine, without which many of our current treatment modalities and medical procedures become exceedingly dangerous. But overuse of antibiotics has made them increasingly ineffective against serious infections.

This antibiotic-resistance has turned into a worldwide health threat of massive proportions that kills tens of thousands every year. One infection, Methicillin resistant Staphylococcus aureus (MRSA), kills more Americans each year than the combined total of emphysema, HIV/AIDS, Parkinson’s disease, and homicide. Solutions for this include improved infection prevention, more responsible use of antibiotics in human medicine, limiting use of antibiotics in agriculture, and finding innovative approaches to treat infections.

But in the wake of this crisis, a good thing has emerged: the re-discovery of natural infection-fighting methods. From garlic to cinnamon to probiotics and fermented foods, to sunlight and Manuka honey, there are positive things in nature that are turning out to be good combatants for fighting infections.

Manuka honey has even been shown to be more effective than antibiotics in the treatment of more than 250 clinical strains of bacteria as well as serious, hard-to-heal, antibiotic-resistant skin infections, including MRSA.

ARB Therapy May Slow Emphysema Progression

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A subset of patients with chronic obstructive pulmonary disease (COPD) with emphysema appeared to benefit from treatment with an angiotensin receptor blocker, supporting preclinical evidence of efficacy, a randomized clinical study suggested.
Overall, patients with COPD treated with losartan (Cozaar) had no improvement compared with placebo-treated patients. However, the subset of patients with emphysema at baseline had stabilization of emphysema at 6 months, whereas patients in the placebo group exhibited a 3% rate of progression (P=0.042). Anatomic analysis also showed a significant difference for the left upper lobe in favor of losartan (P=0.049).

At 12 months, the overall trend toward stability persisted in the patients who had emphysema at baseline but was no longer significant. The anatomical analysis showed a consistent pattern of stability with losartan versus progression with placebo, achieving statistical significance in the right middle lobe, Allison Lambert, MD, of Johns Hopkins, reported here at CHEST 2015.
“From these data, we conclude that, among patients with COPD who have CT-defined emphysema, losartan has the potential to prevent emphysema progression,” said Lambert. “Our secondary outcomes were unchanged.
“The next step in our line of clinical investigation will be to conduct a phase III clinical trial, supported by the NIH Pulmonary Trials Consortium. We anticipate recruiting 220 patients with emphysema, which will afford 90% power to detect differences as identified in our phase II trial.”
The emergence of differences between the groups after a relatively brief treatment period was impressive, but the timing of medication administration and CT scans could influenced findings, suggested Jay Peters, MD, of the University of Texas Health Science Center in San Antonio.
“One of my concerns is that [the improvement] was in the left upper lobe early on and then the right middle lobe at 12 months,” said Peters. “How did you control the time of day that the CT was done and how did that correlate with the medications? It would seem that somebody who had just taken medication with air trapping could look quite different.”

Alluding to data showing that the right middle lobe is the most common site of progression with CT-defined emphysema, Lambert responded, “I do think that this finding within the right middle lobe at 12-month follow-up is true and perhaps compelling. What was striking to me at the 12-month follow-up was the trend across all lobes; all the lobes had stopped progressing.”
The rationale for using ARBs in emphysema dates back to preclinical studies of Marfan syndrome. Animals with emphysema-like changes in alveoli were treated with losartan, which partly reversed the changes. Subsequent studies in mice showed that losartan attenuated adverse lung effects of cigarette smoke and restored lung architecture.
Relevant clinical studies include a trial of the ARB irbesartan (Avapro) in patients with COPD, leading to some changes associated with improved lung function and architecture. A retrospective case-control study showed a reduction in COPD hospitalization and mortality among patients treated with statins and ARBs.
In her presentation here, Lambert reported findings from a randomized, proof-of-concept study to determine whether losartan would prove or slow the progression of emphysema in patients with COPD. Patients with mild to moderate COPD were randomized to losartan or placebo and followed for 12 months. Outcomes of interest included CT-assessed percent emphysema and airway wall thickness; spirometry, lung volumes, and diffusing capacity of the lung for carbon monoxide; and quality of life/health status.
The final analysis included 106 patients, for whom Lambert reported anatomic and functional outcomes. In the overall population, patients assigned to losartan did no better than those in the placebo group with respect to any of the outcomes at 6 or 12 months. However, a prespecified analysis of patients with CT-confirmed emphysema at baseline (n=46) showed anatomical changes favoring the losartan group.

At 6 months, total-lung emphysema had decreased by 0.78% in the losartan group and increased by 3.03% in the placebo group (P=0.042). The lobe-specific anatomic analysis showed a 0.86% decrease in emphysema in the left upper lobe among patients treated with losartan versus an increase of 2.97% in the placebo group (P=0.049). Other lobe-specific values did not differ significantly between the groups, nor did any of the functional outcomes assessed.
At 12 months, patients in the losartan group still had an overall decrease in emphysema (-0.32%) compared with an increase of 2.18% in the placebo group, but the difference was no longer significant (P=0.064). Emphysema in the right middle lobe had decreased by 0.72% in the losartan group but increased by 3.34% in the placebo group (P=0.019).
All of the other lobe-specific assessments showed stable disease in the losartan arm versus 2% to 3% emphysema progression with placebo, although the differences did not achieve statistical significance. None of the functional outcomes differed significantly between treatment groups.