Rationale: Recent U.S. data suggest an increased risk of work-related asthma among health care workers, yet only a few specific determinants have been elucidated. Objectives: To evaluate associations of asthma prevalence with occupational exposures in a cross-sectional survey of health care professionals. Methods: A detailed questionnaire was mailed to a random sample (n ϭ 5,600) of all Texas physicians, nurses, respiratory therapists, and occupational therapists with active licenses in 2003. Information on asthma symptoms and nonoccupational asthma risk factors obtained from the questionnaire was linked to occupational exposures derived through an industry-specific job-exposure matrix. Measurements: There were two a priori defined outcomes: (1 ) physiciandiagnosed asthma with onset after entry into health care ("reported asthma") and (2 ) "bronchial hyperresponsiveness-related symptoms," defined through an 8-item symptom-based predictor.
Conclusions:The contribution of occupational exposures to asthma in health care professionals is not trivial, meriting both implementation of appropriate controls and further study.
the NHANES III project. After excluding subjects with physician-diagnosed emphysema, a total of 18,393 subjects were included in the final analysis.The prevalence of current asthma (asthma) was 4.5% and the prevalence of wheezing in the previous 12 months (wheezing) was 16.4%. Mexican-Americans exhibited the lowest prevalence of asthma when compared with other race/ethnic groups. Multiple logistic regression analysis showed that Mexican-Americans were less likely to report asthma when compared to non-Hispanic whites. Low education level, female sex, current and past smoking status, pet ownership, lifetime diagnosis of physician-diagnosed hay fever and obesity were all significantly associated with asthma and/or wheezing. No significant effect of indoor air pollutants, as derived from the use of household heating/ cooking appliances, on asthma and wheezing was observed in this study.In conclusion, this study observed racial/ethnic differences in the prevalence of asthma and wheezing and identified several important risk factors that may contribute to development and/or exacerbation of asthma and wheezing. Contrary to earlier reports, the proxy measures of indoor air pollution used in this study were not found to be associated with increased risk of asthma and wheezing.
The development of emphysema in humans and mice exposed to cigarette smoke is promoted by activation of an adaptive immune response. Lung myeloid dendritic cells (mDCs) derived from cigarette smokers activate autoreactive Th1 and Th17 cells. mDC-dependent activation of T cell subsets requires expression of the SPP1 gene, which encodes osteopontin (OPN), a pleiotropic cytokine implicated in autoimmune responses. The upstream molecular events that promote SPP1 expression and activate mDCs in response to smoke remain unknown. Here, we show that peroxisome proliferator-activated receptor γ (PPARG/Pparg) expression was downregulated in mDCs of smokers with emphysema and mice exposed to chronic smoke. Conditional knockout of PPARγ in APCs using Cd11c-Cre Pparg flox/flox mice led to spontaneous lung inflammation and emphysema that resembled the phenotype of smoke-exposed mice. The inflammatory phenotype of Cd11c-Cre Pparg flox/flox mice required OPN, suggesting an antiinflammatory mechanism in which PPARγ negatively regulates Spp1 expression in the lung. A 2-month treatment with a PPARγ agonist reversed emphysema in WT mice despite continual smoke exposure. Furthermore, endogenous PPARγ agonists were reduced in the plasma of smokers with emphysema. These findings reveal a proinflammatory pathway, in which reduced PPARγ activity promotes emphysema, and suggest that targeting this pathway in smokers could prevent and reverse emphysema.
This study adds evidence to the literature that identifies work-related asthma as an important public health problem. Several occupations are targeted for additional evaluation and study. Of particular interest are cleaners, which are being increasingly reported as a risk group for asthma. Future intervention strategies need to be developed for effective control and prevention of asthma in the workplace.
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