Smoking cessation can reverse some of the lung damage that occurs among asthma sufferers from smoking cigarettes. Martine Broekema, Ph.D., of the University of Groningen in The Netherlands is lead author of the study published recently in the American Journal of Respiratory and Critical Care Medicine. Broekema said that stopping smoking can reverse thickness in the airways of asthma patients, leading to less mucous production and inflammation.
“We found that exposure to cigarette smoke appears to increase the thickness of the epithelium, or lining, of the airways in the lung. This may be the underlying cause of the fact that smoking asthma patients experience more asthma symptoms, such as shortness of breath and phlegm production, compared to non-smoking asthma patients,” Broekema said.
Studying patients with asthma showed that years and amount of smoking had no bearing on lung changes in asthma patients who stopped smoking. “To our surprise, these two sub-groups of ex-smokers showed no difference in any outcome measure. These sub-analyses indicate that the amount of smoke exposure in the past does not influence our outcome measures,” said Dr. Broekema. “This study shows again how important smoking cessation is for pulmonary health, and this appears to be especially true for asthmatic patients. The good news is that quitting appears to have a measurable benefit in these individuals. “
Current smokers with asthma were found to have more mucous production overall, and more cells that produce mucous. The authors say …”our data suggest that smoking cessation can reverse the thickening of the lining of the airways”.
Asthma patients who stop smoking, regardless of how many years or how many cigarettes, can benefit by smoking cessation. Smoking cessation can reverse thickening of lung tissue, and inflammatory lung change in patients with asthma.
Ozone , traffic pollution increase asthma hospitalizations in children
Both ozone and primary pollutants from traffic substantially increase asthma-related emergency department visits in children, especially during the warm season, according to researchers at the Rollins School of Public Health at Emory University in Atlanta.
Asthma exacerbations are known to be triggered by air pollutants, but researchers are still trying to identify which specific pollutants are to blame, and the extent to which they increase pediatric emergency department visits for asthma.
The researchers obtained data on metropolitan Atlanta emergency department visits for asthma exacerbations in children between five and 17 years of age between 1993 and 2004 and used data on surrounding area pollutants collected as part of the Study of Particles and Health in Atlanta (SOPHIA). They then analyzed the more than 90,000 asthma-related pediatric emergency department visits with respect to the ambient levels of 11 different pollutants. The availability of daily monitoring data on particulate matter components allowed them to develop a detailed picture of pollutant concentrations and subsequent effects on emergency department visits for pediatric asthma exacerbations.
Ozone was strongly associated with an increase in pediatric asthma exacerbations during the summer, and there was evidence of a dose-response relationship beginning with concentrations as low as 30 parts per billion.
Ozone concentrations in many urban areas throughout the U.S., including metropolitan Atlanta, routinely exceed the EPA standard.
“In this study we observed evidence that ambient concentrations of ozone and primary pollutants from traffic sources independently contributed to the burden of emergency department visits for pediatric asthma,” said lead author Matthew J. Strickland, Ph.D., M.P.H., assistant professor of environmental health. “Further, the associations were present at relatively low ambient concentrations, reinforcing the need for continued evaluation of the EPA’s National Ambient Air Quality Standards to ensure that the standards are sufficient to protect susceptible individuals.”
Several markers of pollution from combustion engines—i.e., pollutants emitted from the tailpipes of cars and trucks—were also associated with pediatric emergency department visits for asthma exacerbations during the warm season. When they analyzed the effects of multiple pollutants together, the researchers found evidence that ozone and primary pollutants from traffic sources independently affected pediatric asthma exacerbations.
The findings were published online by the American Thoracic Society’s Web site ahead of the print edition of the American Journal of Respiratory and Critical Care Medicine.
Stress during pregnancy may increase offspring’s asthma risk
Stress during pregnancy may raise the risk of asthma in offspring, according to researchers at Brigham and Women’s Hospital and Harvard Medical School in Boston. The researchers investigated differences in immune function markers in cord blood between infants born to mothers in high stress environments and those born to mothers with lower stress and found marked differences in patterns that may be associated with asthma risk later in life.
“This is the first study in humans to show that increased stress experienced during pregnancy in these urban, largely minority women, is associated with different patterns of cord blood cytokine production to various environmental stimuli, relative to babies born to lower-stressed mothers,” said Rosalind Wright, M.D., M.P.H., associate physician at Brigham and Women’s Hospital.
The findings have been published online ahead of print publication in the American Thoracic Society’s American Journal of Respiratory and Critical Care Medicine.
Asthma is known to be more prevalent among ethnic minorities and among disadvantaged urban communities, but the disparity is not completely explained by known physical factors. Urban women living in the inner-city also experience significant stress, particularly minority women.
Dr. Wright and colleagues recruited pregnant women in several sites, including Boston, Baltimore, New York and St. Louis. Their families were largely ethnic minorities, 20 percent of whom were living below the poverty level. Each child’s mother or a father had a history of asthma or allergy.
In total, 557 families answered detailed questions about the various stressors in their lives, at home (including domestic violence), in their financial situations and in their neighborhoods (community violence). When the infants were born, their cord blood was collected and isolated immune cells were stimulated with a number of factors (allergens like dust and cockroach, viral and bacterial stimulants). Participants were then analyzed for the production of various cytokines as indicators of how the child’s immune system was primed to respond to the environment.
The researchers found that the patterns of cytokines related to certain stimulants differed based on the level of stress mothers reported.
“The ctyokine patterns seen in the higher stress groups, which are an indication of how the child’s immune system is functioning at birth, may be a marker of increased risk for developing asthma and allergy as they get older,” explained Dr. Wright.
“For example, while the debate continues as to whether primary sensitization to allergens begins before birth, these findings suggest the possibility that prenatal stress may enhance the neonates’ response to inhalant antigens, specifically those antigens that the fetus is likely to encounter more directly in utero, like dust mite.”
The research, a prospective cohort study funded by the National Institute of Allergy and Infectious Diseases, will continue as the infants grow up to determine whether maternal stress levels do indeed have an impact on asthma development.
“The current findings suggest that psychological stress is involved in programming of the infant immune response and that this influence begins during pregnancy,” said Dr. Wright. “As these infants mature, we will learn how these factors manifest later in terms of the development of asthma and allergy.”
Food allergy-related disorder linked to master allergy gene
Scientists have identified a region of a human chromosome that is associated with a recently recognized allergic disease known as EoE, short for eosinophilic esophagitis. People with EoE frequently have difficulty eating or may be allergic to one or more foods. This study further suggests that a suspected so-called master allergy gene may play a role in the development of this rare but debilitating disorder.
A symptom of EoE is inflammation of the esophagus and the accumulation of a specific type of immune cell, called an eosinophil. And symptoms vary with age. In young children, a major symptom is spitting up food, while in older children and adults, the condition may cause food to become stuck in the esophagus. These symptoms may improve when a person with EoE is restricted to a liquid formula diet that contains no protein allergens or is placed on a diet that lacks six highly allergenic foods, which are milk, soy, eggs, wheat, peanut and seafood.
Little is known about what causes EoE, but the disease runs in families suggesting that specific genes may be involved.
Investigators at Cincinnati Children’s Medical Center performed a genome-wide association analysis in children with EoE and healthy children. Researchers identified changes in genes within a region on chromosome 5 that were highly associated with EoE. One of the genes in this region encodes a protein called TSLP (thymic stromal lymphopoietin). Investigators found higher levels of TSLP in children with EoE, suggesting that TSLP plays some role in EoE.
TSLP is made by epithelial cells, which line internal and external surfaces of the body. It has already been described as a master switch that may turn on other allergic diseases, such as asthma and atopic dermatitis (eczema).
