Rationale:
Prior studies comparing abnormalities in pulmonary function between HIV-infected and HIV-uninfected persons in the current era are limited.
Objectives:
To determine the pattern and severity of impairment in pulmonary function in HIV-infected compared to HIV-uninfected individuals.
Methods:
Cross-sectional analysis of 300 HIV-infected and 289 HIV-uninfected men enrolled from 2009-2011 in two clinical centers of the Lung HIV Study. Participants completed pre- and post-bronchodilator spirometry, diffusing capacity (DLCO) measurement, and standardized questionnaires.
Results:
Most participants had normal airflow; 18% of HIV-infected and 16% of HIV-uninfected men had airflow obstruction. The mean percent predicted DLCO was 69% in HIV-infected vs. 76% in HIV-uninfected men (p<0.001). A moderately to severely reduced DLCO of ≤60% was observed in 30% of HIV-infected compared to 18% of HIV-uninfected men (p<0.001), despite the fact that 89% of those with HIV were on antiretroviral therapy. A reduced DLCO was significantly associated with HIV and CD4 cell count in linear regression adjusting for smoking and other confounders. The DLCO was lowest in HIV-infected men with CD4 cell counts <200 compared to those with CD4 cell counts ≥200 and to HIV-uninfected men. Respiratory symptoms of cough, phlegm and dyspnea were more prevalent in HIV-infected patients particularly those with abnormal pulmonary function compared to HIV-uninfected patients.
Conclusions:
HIV infection is an independent risk factor for reduced DLCO, particularly in individuals with a CD4 cell count below 200. Abnormalities in pulmonary function among HIV-infected patients manifest clinically with increased respiratory symptoms. Mechanisms accounting for the reduced DLCO require further evaluation.
We assessed the relative impact of residential exposure to community air pollution and habitual cigarette smoking on lung function by comparing the annualized rate of change in forced expiratory volume in 1 s (FEV1) in current, former, and never-smokers 25 to 59 yr of age residing in three demographically similar areas of the Southern California air basin who had been chronically exposed to (1) moderate levels of photochemical oxidants and very low levels of other pollutants (Lancaster); (2) very high levels of photochemical oxidants, sulfates, and particulate matter (Glendora); and (3) high levels of sulfates, oxides of nitrogen, and probably hydrocarbons (Long Beach), together with moderate levels of sulfur dioxide. Of the 621 to 763 nonsmokers, 317 to 479 former smokers and 472 to 691 continuing smokers residing in the three areas who were studied initially, 53 to 64, 49 to 59, and 43 to 54%, respectively, were retested. For male residents, area of residence and smoking category each had highly significant effects on FEV1 decline (two-way ANCOVA; p < 0.001) without significant interaction (p > 0.4). After adjustment for baseline FEV1, age, height, and a history of allergy, the mean decline in FEV1 attributable to living in Long Beach compared with living in Lancaster was 23.6 ml/yr, which was 71% of the rate of decline in FEV1 (33.3 ml/yr), attributable to smoking > 1 pack of cigarettes per day. For female residents, a significant interaction was noted between area and smoking (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
To validate a senile dementia survey diagnostic tool, 195 individuals aged 61-91 and referred by their physicians as normal or mildly demented were examined. The etiologic diagnosis used as criterion was the consensus of two experienced neurologists, assisted by clinical and laboratory data from referring physicians and by neuropsychologic evaluation of questionably affected persons. Agreement between the neurologists was high, as indicated by a weighted Kappa coefficient of 0.97 (95% confidence interval (Cl) (0.94, 1.00)). Agreement between the instrument and criterion diagnosis was also excellent (kappa w = 0.93; 95% Cl (0.88, 0.98)). Used alone as a screening diagnostic tool, the cognitive function portion of the instrument was much more sensitive (0.929) than previously used brief tests and was acceptably specific (0.800). Because normals complete this cognitive test in 15-20 minutes, it should be a major advance in population-based studies of senile dementia and normal aging.
Two never-smoking cohorts in Southern California, one in Lancaster (N = 2340) exposed only to moderate levels of oxidants and the other in Long Beach (N = 1326) exposed to high levels of SOx, NO2, hydrocarbons and particulates completed spirometry and the single-breath nitrogen test five to six years apart. Forty-seven percent and 45 percent of the participants were retested. Mean results at baseline for those tested and not retested were similar. Loss to follow-up was primarily due to moving (39 percent and 47 percent). Every difference of consequence indicated greater deterioration in lung function in Long Beach. The level of significance of the difference was greatest, even in the youngest age groups, for delta N2(750-1250), suggesting that the earliest site of impairment may occur in the small airways. Greater deterioration in spirometric parameters was observed in every age group in Long Beach females above seven years of age at baseline and in Long Beach males above 15 years of age, suggesting that chronic exposure to the pollutant mix occurring in Long Beach ultimately adversely affects the large airways as well as small airways.
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