American journal of respiratory and critical care medicine
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Am. J. Respir. Crit. Care Med. · Feb 2001
Effects of maternal smoking during pregnancy and environmental tobacco smoke on asthma and wheezing in children.
The effects of maternal smoking during pregnancy and childhood environmental tobacco smoke (ETS) exposure on asthma and wheezing were investigated in 5,762 school-aged children residing in 12 Southern California communities. Responses to a self- administered questionnaire completed by parents of 4th, 7th, and 10th grade students were used to ascertain children with wheezing or physician-diagnosed asthma. Lifetime household exposures to tobacco smoke were assessed using responses about past and current smoking histories of household members and any history of maternal smoking during pregnancy. ⋯ We conclude that maternal smoking during pregnancy increases the occurrence of physician-diagnosed asthma and wheezing during childhood. In contrast, current ETS exposure is associated with wheezing, but not physician-diagnosed asthma. Taken together, our findings support the hypothesis that ETS operates as a cofactor with other insults such as intercurrent infections as a trigger of wheezing attacks, rather than as a factor that induces asthma, whereas in utero exposure acts to increase physician-diagnosed asthma
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Am. J. Respir. Crit. Care Med. · Feb 2001
Granulocyte inflammatory markers and airway infection during acute exacerbation of chronic obstructive pulmonary disease.
There is increasing evidence that chronic obstructive pulmonary disease (COPD) is associated with chronic inflammation in the airways and lung parenchyma; however, little is known about the inflammatory response during acute COPD exacerbation. The objectives of this study were (1) to determine if inflammatory markers associated with neutrophilic inflammation and activation increase at times of acute COPD exacerbation relative to the clinically stable state, and (2) to determine whether the presence of acute bacterial or viral infection at the time of COPD exacerbation could be correlated with increases in sputum markers of inflammation. Induced sputum was collected from patients with COPD when they were clinically stable, during the time of an acute exacerbation, and 1 mo later. ⋯ Three of 14 patients (21%) had confirmed bacterial or viral respiratory tract infections. Patients with documented infection did not demonstrate greater increases in sputum levels of inflammatory cytokines during exacerbations compared with patients without demonstrable infection. We conclude that markers of airway neutrophilic inflammation increase at the time of acute COPD exacerbation and then decline 1 mo later, and that this acute inflammatory response appears to occur independently of a demonstrable viral or bacterial airway infection.
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Am. J. Respir. Crit. Care Med. · Feb 2001
Abnormal sleep/wake cycles and the effect of environmental noise on sleep disruption in the intensive care unit.
Little is known about sleep/wake abnormalities in intensive care and less is known about the mechanisms responsible for these abnormalities. We studied 22 (20 mechanically ventilated) medical intensive care unit (ICU) patients with continuous polysomnography (PSG) and environmental noise measurements for 24-48 h to characterize sleep-wake patterns and objectively determine the effect of environmental noise on sleep disruption. All 22 patients demonstrated sleep-wake cycle abnormalities. There were large variations in total sleep time (TST) with the mean total sleep time per 24-h study period of 8.8 +/- 5.0 h. Sleep-wake cycles were fragmented and nonconsolidated with a mean of 57 +/- 18% and 43 +/- 18% of the TST occurring during the day and night, respectively. Environmental noise was responsible for 11.5 and 17% of the overall arousals and awakenings from sleep, respectively. The mean noise arousal index was 1.9 +/- 2.1 arousals/h sleep. ⋯ (1) ICU patients are qualitatively, but not necessarily quantitatively, sleep deprived; and (2) although environmental noise is in part responsible for sleep-wake abnormalities, it is not responsible for the majority of the sleep fragmentation and may therefore not be as disruptive to sleep as the previous literature suggests.