American journal of respiratory and critical care medicine
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Am. J. Respir. Crit. Care Med. · Jun 1995
Comparative StudyEffects of smoking and smoking cessation on longitudinal decline in pulmonary function.
Effects of cigarette smoking and smoking cessation on rate of FEV1 decline over 6 yr were examined in 4,451 Japanese-American men from the Honolulu Heart Program who were 45 to 68 yr of age at baseline (1965-1968). Within-person regression was used to calculate annual change in FEV1. Rates of FEV1 decline varied strongly with smoking status and increased significantly with age. ⋯ Among 216 men with impaired pulmonary function, those who quit smoking had significantly slower rates of FEV1 decline than did those who continued smoking. Potential reasons for quitting included respiratory conditions and stroke. These results extend previous reports of accelerated rates of FEV1 decline in the persons who continue to smoke, and they indicate that smoking cessation leads to less steep rates of decline in pulmonary function over a short period of time in middle-aged men, as well as in men with established pulmonary impairment.
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Am. J. Respir. Crit. Care Med. · May 1995
Cigarette smoke inhibits lung fibroblast proliferation and chemotaxis.
Cigarette smoking is the most clearly recognized cause of pulmonary emphysema. Since loss of lung tissue, which characterizes emphysema, represents a balance between injury and repair, we hypothesized that cigarette smoke might contribute to the development of emphysema by inhibiting fibroblast proliferation and migration. To evaluate this, we examined the effect of cigarette smoke extract (CSE) on the proliferation and migration of human lung fibroblasts in vitro. ⋯ Therefore, we also examined acrolein and acetaldehyde, which are volatile components of cigarette smoke, Micromolar concentrations of acrolein and millimolar concentrations of acetaldehyde induced significant inhibition of fibroblast proliferation. In contrast, removal of volatile components did not eliminate the inhibitory activity of CSE for fibroblast migration, although acetaldehyde and acrolein alone were also capable of inhibiting chemotaxis. Cigarette smoke-induced inhibition of fibroblast proliferation and migration may impair lung repair following lung injury, and may thus contribute to the development of pulmonary emphysema.
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Am. J. Respir. Crit. Care Med. · May 1995
Do lower respiratory tract infections in early childhood cause chronic obstructive pulmonary disease?
The hypothesis that lower respiratory tract infections (LRTI) in early childhood lead to chronic obstructive pulmonary disease (COPD) in late adult life has been difficult to test. However, a unique opportunity arose when records were discovered in the counties of Hertfordshire and Derbyshire, England, that contained information about childhood LRTI recorded 60 to 70 years ago. The lung function of some men still living in these counties was examined. ⋯ In Derbyshire men, pneumonia before 2 yr of age was associated with a large and highly significant reduction in mean FEV1, adjusted for age and height. These findings were independent of smoking and social class. These data support a causal relationship between LRTI in early life and subsequent COPD.