Chronic Respiratory Diseases: Challenges in Diagnosis and Prevention

Basil Varkey; Lisa A. Maier

Disclosures

Curr Opin Pulm Med. 2015;21(2):111-113. 

According to the WHO, hundreds of millions of people are affected by chronic respiratory diseases. They cause significant morbidity and mortality; more than 10% of deaths from noncommunicable diseases in 2008 were attributed to respiratory diseases.[1] Regrettably, many of these diseases are preventable as they are caused by inhalant exposures at home and in workplace but may go undiagnosed, diagnosed late in the course or misdiagnosed. There is a need and an opportunity for the practicing physician to reduce the impact of these diseases by understanding their various manifestations, the exposures that cause them and the steps to take to treat and prevent them. To this end, in this edition of Current Opinion in Pulmonary Medicine, a series of articles are presented that reviews the existing knowledge and describes newer findings for clinicians – primary care as well as pulmonary medicine – on chronic respiratory diseases caused by exposures.

Chronic obstructive pulmonary disease (COPD), mostly caused by self-inflicted inhalant exposure to tobacco smoke, tops the list of chronic respiratory diseases in incidence, morbidity and mortality. In the first article of this issue, Jagana et al.[2] explore the reasons for delayed diagnosis of COPD, particularly the underuse of spirometry and propose a trigger of automatic health alert for spirometry in smokers 40 years or older with respiratory symptoms. This is a practical and doable proposal but unfortunately limited in application to affluent countries with electronic medical records. The predominant symptom of COPD patients is dyspnea that causes debilitation and suffering, and Laveneziana et al.[3] explain the components and multiple dimensions of dyspnea.

A vexing and continuing issue for researchers and clinicians alike is the heterogeneity, and marked variations between patients, of COPD.[4] Naturally, more effort was directed at finding and grouping phenotypes within the broad universe of COPD. One such phenotype is chronic bronchitis, the subject of Kim and Criner's article[5] in this issue. Recent report of a major study – Evaluation of COPD Longitudinally to Identify Predictive Surrogate Points (ECLIPSE) – further affirmed the heterogeneity of COPD and advanced our knowledge and challenged our views of COPD in multiple fronts: continued smoking and presence of emphysema predicted progression of the disease, COPD does not cause progressive loss of pulmonary function in all patients, sputum and circulating biomarkers are not ready for use in clinical practice, and evidence for systemic inflammation (as measured by the current methods) is present only in a minority of patients, although persistent inflammation is associated with poor prognosis[6,7] In another notable publication of 2014, prognostic value of multiple indices was compared. A combination of body mass, airflow obstruction, dyspnea and exercise (BODE) index and COPD comorbidity test (COTE) index provided the best indicator for all-cause mortality[8]

Antibiotics and corticosteroids are the mainstays of treating hospitalized patients with acute exacerbations of COPD, and clinicians choose different antibiotics and varying doses of steroids. Often they err on the side of using potent antibiotic and high doses of steroids, as clear evidence-based information on the right choices were scant to absent. Kiser and Vandivier[9] reviewed the evidence and make their recommendations for the rational use of antibiotics and steroids in this issue. A related issue is the use of inhaled steroids in the chronic management of COPD patients and questions related to it: Is inhaled steroid and inhaled long-acting bronchodilator superior to two long-acting bronchodilators (with different pharmacology and different mechanism of action) in prolonging time between acute exacerbations? Can inhaled steroid be safely withdrawn after long-term use? The answers are 'no' to the first question and 'yes' to the second according to the Withdrawal of Inhaled Steroids during Optimized Bronchodilator Management (WISDOM) study.[10] Although the last word on this may not be written, this study is a worthy one on a common and clinically important topic.

Although tobacco use is the most common cause of COPD globally, it is important to recognize that over 15% of COPD cases are attributed to exposures in the workplace and that a substantial portion of nonsmoking adults have COPD, as is described in the article by Bang.[11] Environmental exposures likely have a significant global impact on COPD in nonsmokers with the high levels of air pollution and use of biomass in the home of many developing countries, and COPD is found at higher rates in nonsmokers in many countries outside the USA, supporting this notion. The exposures and other risk factors outlined in this article should be considered as the clinician evaluates the nonsmoking patient with COPD to help determine whether the disease is related to exposures in the workplace or home, as exposure cessation, like tobacco cessation, is prudent.

Unfortunately, as noted in Moitra et al.'s article,[1] as the global use of new technologies, chemical and materials increases, new workplace and environmental induced lung diseases have been discovered and old diseases that were thought to have disappeared have re-emerged. Initially, many exposure-related lung diseases are presented as case reports in medical journals from astute clinicians who questioned the connection between an exposure and lung disease, as noted in numerous articles in this edition.[12–14] Often, these case reports describe severe lung disease and are the 'tip of the iceberg' for an impending outbreak.

This demonstrates the challenge in diagnosing exposure-related respiratory disease; it can be complex and daunting for physicians with many demands and limited time in clinic to make the connection between lung disease and exposure. However, as Drs. Papali and Hines remind us, if you initially ask the patient what they do; how they do it; are they concerned about exposures on or off the job; and whether coworkers are sick (WHAC), the start of an occupational and environmental history may be obtained.[15] Without this history, no connection between exposure and lung disease can be made. As noted by Dr Glazer,[16] if the exposure connection is not made in cases of interstitial lung disease (i.e. hypersensitivity pneumonitis is not considered in the differential of fibrotic lung disease) and the individual is not removed from exposure, their prognosis is markedly worse.

Consideration of the radiographic manifestations can help raise the suspicion of an exposure-related disease as described in detail by Cox and Lynch[12] and Glazer.[16] For example, although some diseases may appear the same clinically, such as smoking-related COPD, chronic bronchitis and respiratory bronchiolitis, radiographic manifestations may help differentiate these diseases. However, it is important to consider exposures other than tobacco use, as these diseases maybe caused by dusts and fumes, such as those experienced by military personnel in deployment in the Middle East, as noted by Krefft et al..[13] Furthermore, an exposure, especially when as complex as those sustained by military deployers in the Middle East, may produce a number of phenotypes or heterogeneity of disease. Finally, all lung disease may be considered idiopathic if the important clinical and pathophysiological connections are not made; without obtaining information about occupational and environmental exposures, the practiced clinician will not be able to take out the 'idiopathic' in idiopathic disease, as is described in depth by Gulati and Redlich.[17] Review of the epidemiological literature conducted to date supports a causative role for specific exposures in the development of idiopathic pulmonary fibrosis, and likely other diseases, although some of these exact exposures have yet to be definitively identified for the individual patient, except for the case of asbestosis.[17]

It is our hope that these articles will increase the clinician's ability to recognize the noninfectious exposure-related respiratory diseases discussed in this journal, along with the disease manifestations and causes. Each of these articles should remind us of the critical link between our environment and the potential development of lung disease; after all, the lung is constantly exposed to the world around us. Hopefully, the reader has an appreciation of the size and scope of the problem, and this increased awareness along with the clinical clues provided herein will prompt us to consider an environmental contribution to lung disease in individual patients, and encourage us to find ways to reduce relevant exposures in ways to limit morbidity and mortality and ultimately prevent disease. In turn, this should allow the clinician to implement appropriate treatment and management to ultimately reduce the impairment,[18] morbidity and mortality associated with these diseases worldwide.

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