News Release

American Thoracic Society journal news tips for May 2005 (first issue)

Peer-Reviewed Publication

American Thoracic Society

ACETAMINOPHEN USE ASSOCIATED WITH ASTHMA, COPD, AND DECREASED LUNG FUNCTION

In a large, cross-sectional study, researchers found that increased use of the pain killer acetaminophen was associated with a greater prevalence of asthma and chronic obstructive pulmonary disease (COPD), as well as directly related to decreased lung function if used daily, according to an article in the first issue for May 2005 of the American Thoracic Society's peer-reviewed American Journal of Respiratory and Critical Care Medicine.

British researchers studied data from 13,492 persons who were part of the Third National Health and Nutrition Survey (NHAMES III), a U.S. study which took place from 1988 to 1994. Among other questions, participants in NHAMES III were asked whether they had taken aspirin, acetaminophen, and ibuprofen during the previous month. Their replies were divided into "never users;" "occasional users" (1 to 5 times in the past month); "regular users" (6 to 29 times during the past month); and "daily users" (more than 29 times during the last month).

According to the researchers, prior animal studies had shown that acetaminophen could deplete an antioxidant found in airway epithelial lung fluid which could ultimately damage the tissue.

The investigators found that the prevalence of asthma was 6.9 percent and that of COPD 11.8 percent in the NHAMES III data. In addition, 2.8 percent had both respiratory diseases. Of the group, about 4 percent of the participants were daily users of acetaminophen as compared with 8.2 percent for aspirin and 2.5 percent for ibuprofen. Approximately 3 percent of the population reported use of all three medications in the last month, and 16 percent had two different types of pain medications.

The researchers said that neither the use of aspirin nor the use of ibuprofen was associated with the prevalence of either asthma or COPD. However, they point out when their results were combined with those of prior investigators, they support the hypothesis that acetaminophen use can cause an increase in asthma risk with potential effects on the onset, progression, and severity of the disease.

FAMILY MEMBERS OF ICU PATIENTS SHOW RISK OF POST-TRAUMATIC STRESS SYNDROME

In a study of 284 family members of patients who were either discharged from or died in 21 French medical-surgical intensive care units (ICUs), one-third of the relatives questioned 90 days after the event showed levels on a test that demonstrated moderate to major risk of post-traumatic stress reaction.

Using the impact of events test, investigators saw even higher rates among family members who felt that they were getting incomplete information from ICU staff (48.4 percent), who had to share in surrogate decision-making (47.4 percent), who had a relative die in the ICU (50 percent), whose relative died after end-of-life decisions (60 percent) and who shared in those end-of-life decisions (81.8 percent).

Post-traumatic stress disorder is a psychological reaction that occurs after experiencing a highly stressful event outside the range of normal human experience. It is usually characterized by depression, anxiety, flashbacks, recurrent nightmares, and avoidance of reminders of the past.

The investigators said that the first step toward improvement might be to determine whether better information for families sharing end-of-life decisions would decrease their risk of post-traumatic stress reaction.

The study appears in the first issue for May 2005 of the American Thoracic Society's peer-reviewed American Journal of Respiratory and Critical Care Medicine.

VITAMIN C SUPPLEMENTATION LIMITS EFFECT OF NICOTINE ON PRIMATE FETAL LUNG TISSUE

Vitamin C supplementation during pregnancy in rhesus monkeys limited the deleterious effects of nicotine exposure to their offspring.

According to the authors, earlier work had pointed out that nicotine from smoking resulted in many serious effects on the fetus during pregnancy. In this study, nicotine in the primate mothers that was equivalent to heavy smoking significantly reduced forced expiratory flows in their offspring's lung function. However, supplementation of the mothers with 250 mg of vitamin C per day during pregnancy prevented the effects on expiratory flow.

Six pregnant rhesus monkeys were randomly allocated to a control group, seven to a nicotine-treated group, and seven to a nicotine plus vitamin C group. The 14 pregnant rhesus monkeys were treated with a pump delivering nicotine bitartrate from gestation days 26 to 160. Seven received 250 mg of vitamin C per day. On gestation day 160 out of a term of 165 days, the fetuses were delivered by C-section. The next day, the infant monkeys were given pulmonary function tests.

The problem of human mothers smoking during pregnancy is a dangerous one, according to the researchers. The fetal lung is particularly sensitive to the effects of maternal smoking. Infants exposed in utero to nicotine have decreased pulmonary function at birth, which can persist throughout childhood and beyond. Despite antismoking campaigns, approximately 12 percent of women smoke during pregnancy, resulting in more than 450,000 smoke-exposed infants born in the U.S. during 2002. They explained that smoking during pregnancy causes premature delivery and intrauterine growth retardation and has been estimated to cause five to ten percent of all fetal and neonatal deaths. The problem of smoking mothers also increases the risk of hospitalizations of their babies for respiratory illness, of childhood asthma, and of dying from sudden infant death syndrome.

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The research is published in the first issue for May 2005 of the American Thoracic Society's peer-reviewed American Journal of Respiratory and Critical Care Medicine.

For the complete text of these articles, please see the American Thoracic Society Online Web Site at http://www.atsjournals.org. For either contact information or to request a complimentary journalist subscription to ATS journals online, or if you would like to add your name to the Society's twice monthly journal e-mail list, contact Cathy Carlomagno at (212) 315-6442, or by e-mail at ccarlomagno@thoracic.org.


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