Geoepidemiology of COPD and idiopathic pulmonary fibrosis

Zeki, Amir A.; Schivo, Michael; Chan, Andrew; Hardin, Kimberly A.; Kenyon, Nicholas J.; Albertson, Timothy E; Rosenquist, Grace L.; Louie, Samuel

doi:10.1016/j.jaut.2009.11.004

Cited by 44 publications

(14 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There is obviously an extensive body of literature and space does not permit all relevant citations. We do note a recent symposia and dedicated issues as part of the Congress of Autoimmunity on this theme [146-187]. Based on the above data and the approaches outlined, we are confident that several environmental exposures contribute to the development of AID (Table 1) and that there is sufficient evidence that other exposures likely contribute to the development of AID (Table 2).…”

Section: Discussionmentioning

confidence: 81%

Epidemiology of environmental exposures and human autoimmune diseases: Findings from a National Institute of Environmental Health Sciences Expert Panel Workshop

Miller

Alfredsson

Costenbader

et al. 2012

Journal of Autoimmunity

284

229

View full text Add to dashboard Cite

Autoimmune diseases (AID) are a collection of many complex disorders of unknown etiology resulting in immune responses to self-antigens and are thought to result from interactions between genetic and environmental factors. Here we review the epidemiologic evidence for the role of environmental factors in the development of human AID, the conclusions that can be drawn from the existing data, critical knowledge gaps, and research needed to fill these gaps and to resolve uncertainties. We specifically summarize the state of knowledge and our levels of confidence in the role of specific agents in the development of autoimmune diseases, and we define the areas of greatest impact for future investigations. Among our consensus findings we are confident that: 1) crystalline silica exposure can contribute to the development of several AID; 2) solvent exposure can contribute to the development of systemic sclerosis; 3) smoking can contribute to the development of seropositive rheumatoid arthritis; and 4) an inverse association exists between ultraviolet radiation exposure and the risk of development of multiple sclerosis. We suggest that more studies of phenotypes, genotypes, and multiple exposures are needed. Additional knowledge gaps needing investigation include: defining important windows in the timing of exposures and latencies relating to age, developmental state, and hormonal changes; understanding dose-response relationships; and elucidating mechanisms for disease development. Addressing these essential issues will require more resources to support research, particularly of rare AID, but knowledge of the risks conferred by environmental factors in specific genetic contexts could pave the way for prevention of AID in the future.

show abstract

Section: Discussionmentioning

confidence: 81%

Epidemiology of environmental exposures and human autoimmune diseases: Findings from a National Institute of Environmental Health Sciences Expert Panel Workshop

Miller

Alfredsson

Costenbader

et al. 2012

Journal of Autoimmunity

284

229

View full text Add to dashboard Cite

show abstract

“…Further investigations into the mechanisms for relevance of COPD with the development of lung cancer are warranted. Moreover, because smoking habit varies largely between different genders and estrogen and autoimmunity were possibly associated with lung diseases [71], further investigations in studies powered to evaluate men and women separately might help to identify more details in the pathogenesis of lung cancer.…”

Section: Discussionmentioning

confidence: 99%

Association between Chronic Obstructive Pulmonary Disease and Lung Cancer: A Case-Control Study in Southern Chinese and a Meta-Analysis

et al. 2012

View full text Add to dashboard Cite

BackgroundLung cancer and chronic obstructive pulmonary disease (COPD) share a common risk factor in cigarette smoking and a large portion of patients with lung cancer suffer from COPD synchronously. We therefore hypothesized that COPD is an independent risk factor for lung cancer. Our aim was to investigate the intrinsic linkage of COPD (or emphysema, chronic bronchitis and asthma) and lung cancer.MethodsThe present hospital-based case-control study included 1,069 patients with newly diagnosed lung cancer and 1,132 age frequency matched cancer-free controls. The odds ratios (ORs) for the associations between each previous pulmonary disease and lung cancer were estimated with logistic regression models, adjusting for age, sex, family history of cancer, BMI and pack year smoking. In meta-analysis, the pooled effects of previous pulmonary diseases were analyzed with random effects models; and stratification analyses were conducted on smoking status and ethnicity.ResultsIn the case-control study, previous COPD was associated with the odds for increased risk of lung cancer (OR = 1.29, 95% confidence interval [CI] = 1.00∼1.68); so were emphysema (OR = 1.55, 95%CI = 1.03∼2.32) and chronic bronchitis (OR = 1.22, 95%CI = 0.99∼1.67); while asthma was associated with odds for decreased risk of lung cancer (OR = 0.29, 95%CI = 0.16∼0.53). These associations were more pronounced in smokers (P<.05 for all strata), but not in non-smokers. In meta-analysis, 35 studies (22,010 cases and 44,438 controls) were identified. COPD was significantly associated with the odds for increased risk of lung cancer (pooled OR = 2.76; 95% CI = 1.85–4.11), so were emphysema (OR = 3.02; 95% CI = 2.41–3.79) and chronic bronchitis (OR = 1.88; 95% CI = 1.49–2.36); and these associations were more pronounced in smokers than in non-smokers (P<.001 respectively). No significant association was observed for asthma.ConclusionPrevious COPD could increase the risk of lung cancer, especially in smokers.

show abstract

“…Approximately 20 million adults in the USA have COPD, with a mortality of 20 out of 100 000 [2]. The most common cause of COPD in the general population is cigarette smoking [2, 3]. Persistent inflammation is a key component of COPD pathogenesis.…”

Section: Introductionmentioning

confidence: 99%

Simvastatin inhibits smoke-induced airway epithelial injury: implications for COPD therapy

Davis¹,

Zeki

Bratt³

et al. 2012

Eur Respir J

Self Cite

View full text Add to dashboard Cite

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death. The statin drugs may have therapeutic potential in respiratory diseases such as COPD, but whether they prevent bronchial epithelial injury is unknown. We hypothesised that simvastatin attenuates acute tobacco smoke-induced neutrophilic lung inflammation and airway epithelial injury. Spontaneously hypertensive rats were given simvastatin (20 mg·kg−1 i.p.) daily for either 7 days prior to tobacco smoke exposure and during 3 days of smoke exposure, or only during tobacco smoke exposure. Pre-treatment with simvastatin prior to and continued throughout smoke exposure reduced the total influx of leukocytes, neutrophils and macrophages into the lung and airways. Simvastatin attenuated tobacco smoke-induced cellular infiltration into lung parenchymal and airway subepithelial and interstitial spaces. 1 week of simvastatin pre-treatment almost completely prevented smoke-induced denudation of the airway epithelial layer, while simvastatin given only concurrently with the smoke exposure had no effect. Simvastatin may be a novel adjunctive therapy for smoke-induced lung diseases, such as COPD. Given the need for statin pre-treatment there may be a critical process of conditioning that is necessary for statins’ anti-inflammatory effects. Future work is needed to elucidate the mechanisms of this statin protective effect.

show abstract

Geoepidemiology of COPD and idiopathic pulmonary fibrosis

Cited by 44 publications

References 54 publications

Epidemiology of environmental exposures and human autoimmune diseases: Findings from a National Institute of Environmental Health Sciences Expert Panel Workshop

Epidemiology of environmental exposures and human autoimmune diseases: Findings from a National Institute of Environmental Health Sciences Expert Panel Workshop

Association between Chronic Obstructive Pulmonary Disease and Lung Cancer: A Case-Control Study in Southern Chinese and a Meta-Analysis

Simvastatin inhibits smoke-induced airway epithelial injury: implications for COPD therapy

Contact Info

Product

Resources

About