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Work in the nylon flocking industry poses substantial risk for a previously unrecognized occupational interstitial lung disease. Nylon fiber is the suspected cause of this condition.

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The quantification of human immunodeficiency virus type 1 (HIV-1) RNA has facilitated clinical research and expedited the development of antiretroviral drugs. The branched-DNA (bDNA) assay provides a reliable method for the quantification of HIV-1 RNA in human plasma and is considered one of the most reproducible assays ready for use in clinical trials. A series of oligonucleotide probe design and solution changes have been developed to enhance the sensitivity of the bDNA assay while maintaining its performance characteristics. Among the changes incorporated into the enhanced-sensitivity bDNA (ES bDNA) assay to reduce the background level and enhance the signal are the use of shorter overhang sequences of target probes for capture, the cruciform design of target probes for amplification, and the addition of preamplifier molecules. The ES bDNA assay is at least 20-fold more sensitive than the first-generation bDNA assay, yet it maintains a high level of accuracy, linearity, and reproducibility. Further, quantification values obtained with the ES bDNA assay and the first-generation bDNA assay are highly correlated, thus allowing for meaningful comparisons of HIV-1 RNA levels in specimens tested with either assay. The ES bDNA assay may be useful in determining the prognostic value of HIV-1 RNA levels of below 10,000 copies per ml and in assessing the clinical benefit of antiretroviral therapy-induced decreases in plasma HIV-1 RNA sustained at levels of below 10,000 copies per ml.

The reactive airways dysfunction syndrome (RADS) defines a chronic asthmalike illness with airway hyperresponsiveness that develops within 24 h of a single, brief, highly irritating inhalation exposure. Support for the syndrome has been limited to case reports. A chemical spill, exposing hospital employees to 100% acetic acid, offered an opportunity to more convincingly establish the existence of RADS. All 56 exposed subjects were asked both to complete a questionnaire focusing on their preexposure health status, potential for exposure, and symptom development after the accident, 8 months after the spill, and to undergo methacholine challenge testing to detect airway hyperresponsiveness. An industrial hygienist, blinded to clinical data, estimated each subject's exposure. Preemployment health history forms were reviewed to assess recall bias. The study questionnaire was returned by 51 (91%) subjects; 24 (47%) consented to methacholine challenge, including 7 of the 8 with RADS-consistent symptoms. Diagnostic criteria for RADS were satisfied by none of 7 (0%) subjects with low exposure, 1 of 30 (3.3%) with medium exposure, and 3 of 14 (21.4%) with high exposure (test of trend p value = 0.021). The odds ratio estimate of the relative risk of RADS in subjects with high exposure was 9.8 (95% Cl, 0.902 to 264.6). Neither stratified analysis nor review of the preemployment health history forms revealed evidence of confounding or recall bias, respectively. The reactive airways dysfunction syndrome appears to be a valid clinical entity. Further study of RADS is especially appropriate given increasing evidence that airway inflammation may be etiologically important in all asthma.