Effect of Occupational Exposures on Decline of Lung Function in Early Chronic Obstructive Pulmonary Disease

Harber, Philip; Tashkin, Donald P.; Simmons, Michael; Crawford, Lori; Hnizdo, Eva; Connett, John E.

doi:10.1164/rccm.200605-730oc

Cited by 81 publications

(69 citation statements)

References 40 publications

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“…In the developed world, cigarette smoking is by far the most important risk factor for COPD. Exposure to air pollution particles, occupational exposures to dusts and fumes (39), and, in the developing world, exposure to biomass fuels used for cooking is also believed to be etiological agents of COPD (38).…”

mentioning

confidence: 99%

Animal models of chronic obstructive pulmonary disease

Wright¹,

Cosio²,

Churg³

2008

American Journal of Physiology-Lung Cellular and Molecular Phys

371

326

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-The mechanisms involved in the genesis of chronic obstructive pulmonary disease (COPD) are poorly defined. This area is complicated and difficult to model because COPD consists of four separate anatomic lesions (emphysema, small airway remodeling, pulmonary hypertension, and chronic bronchitis) and a functional lesion, acute exacerbation; moreover, the disease in humans develops over decades. This review discusses the various animal models that have been used to attempt to recreate human COPD and the advantages and disadvantages of each. None of the models reproduces the exact changes seen in humans, but cigarette smoke-induced disease appears to come the closest, and genetically modified animals also, in some instances, shed light on processes that appear to play a role. chronic obstructive pulmonary disease CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) is an increasingly important cause of morbidity and mortality. COPD is now the fifth leading cause of death worldwide (109), and recent estimates suggest that the prevalence is as high as 9 -10% of adults over age 40 (38, 131). In the developed world, cigarette smoking is by far the most important risk factor for COPD. Exposure to air pollution particles, occupational exposures to dusts and fumes (39), and, in the developing world, exposure to biomass fuels used for cooking is also believed to be etiological agents of COPD (38).There are few animal models of COPD related to air pollution particles, dusts and fumes, and biomass fuels; most COPD models have either used cigarette smoke or other approaches, including genetic modifications to mice, believed to reproduce some of the mechanisms behind cigarette smoke. We have recently reviewed mechanistic studies of smoke-exposed animal models (16). In this paper, we will focus on the pros and cons of different COPD animal models.The first question to ask in this context is what would constitute a perfect model of human COPD. This is not a simple question because human COPD consists of at least four anatomic lesions (further defined below): emphysema, small airway remodeling (including goblet cell metaplasia), chronic bronchitis, and pulmonary hypertension; a given patient may have any or all of these lesions. In addition, COPD patients may develop acute exacerbations that are believed to have an infectious basis. To further complicate matters, no matter which lesions are present, COPD develops and is slowly progressive over many years.Because COPD is closely related to the underlying anatomy of the lung, a good animal model should have pulmonary anatomy similar to that of humans. The fundamental mechanisms behind COPD should be similar in animal models and humans. The ideal model would allow the investigator to produce the various different anatomic lesions just listed, all in a short period of time. Unfortunately, all of the known animal models meet only some of the above criteria, and even another human would probably not meet all of them, because, as noted above, there is considerable human to human variation in th...

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mentioning

confidence: 99%

Animal models of chronic obstructive pulmonary disease

Wright¹,

Cosio²,

Churg³

2008

American Journal of Physiology-Lung Cellular and Molecular Phys

371

326

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“…A signifi cant part of the literature accumulated over the past two decades demonstrated the relationship between vapour, gases, dust, and fumes (VGDF) and the development of COPD (7)(8)(9)(10)(11)(12)(13). However its importance remains underappreciated, especially in the Russian Federation.…”

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confidence: 99%

Copd and occupation: a retrospective cohort study of industrial workers

Мазитова

Saveliev

Berheeva

et al. 2012

Archives of Industrial Hygiene and Toxicology

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The aim of this paper was to ascertain chronic obstructive pulmonary disease (COPD) prevalence among industrial workers in the Russian Federation and determine relative contribution of smoking and occupational factors to COPD. We recruited 1,375 workers aged 30 or over. Six hundred and twenty-four of them were occupationally exposed to vapours, gases, dust, and fumes (VGDF). Physical examination and baseline spirometry were performed for all the participants of the study. Those with airfl ow limitation of FEV 1 /FVC<0.70 were considered having COPD and those with presence of cough and sputum production for at least three months in each of two consecutive years were considered having chronic bronchitis (CB), with no overlapping between these 2 groups. Data on occupational history and VGDF levels in the working area were collected from all participants. In total, 105 cases of COPD and 170 cases of CB were diagnosed in the cohort of examined workers. Occupational exposure to VGDF was twice as often present among COPD patients than among both patients with CB and the control group of healthy workers (p<0.05). More than 40 % of COPD patients were occupationally exposed to VGDF above the value of 3.0 of the occupational exposure limit (OEL) and more than 20 % to 6.0 OEL and higher. Overall odds ratio for COPD development due to occupational VGDF exposure was 5.9 (95 % CI=3.6 to 9.8, p=0.0001). Both smoking and VGDF seem to be important for the development of COPD. Analysis of the combined effect of tobacco smoking and occupational noxious particles and gases on COPD development has shown the following order of risk factors based on the strength of their infl uence: VGDF levels, smoking index, age, and heating microclimate. There is a statistically signifi cant level of relationship and "dose-effect" dependence between occupational exposures to VGDF and the development of COPD. The effect of VGDF composition on the probability of COPD development was not found in the study. Results of this study were used to substantiate the inclusion of COPD into the National List of Occupational Diseases of the Russian Federation.

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“…Cigarette smoking is the major aetiological factor for the development of COPD, with exposure to pollution, dust or fumes contributing to a much lesser extent [3]. Despite the understanding that cigarette smoke is a causative agent, since .90% of COPD patients are current or former smokers [4], the mechanism by which cigarette smoke leads to COPD is not well understood.…”

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confidence: 99%

Mechanisms of clearance of nontypeable Haemophilus influenzae from cigarette smoke-exposed mouse lungs

Gaschler¹,

Zavitz²,

Bauer³

et al. 2010

European Respiratory Journal

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Inflammation is prevalent in all stages of chronic obstructive pulmonary disease, and, furthermore, individuals undergo periods of exacerbation, during which pulmonary inflammation increases, often a result of bacterial infection. The present study investigates the in vivo consequences of cigarette smoke exposure on bacterial challenge with nontypeable Haemophilus influenzae (NTHi).BALB/c and C57 black 6 (C57BL/6) mice were exposed to cigarette smoke once or twice daily for a total period of 8 weeks.Exacerbated inflammation was observed in cigarette smoke-exposed compared to room-airexposed mice following challenge with live or heat-inactivated NTHi. Accelerated clearance of live NTHi from cigarette smoke-exposed mice was independent of the establishment of chronic inflammation or direct toxic effects of cigarette smoke components on bacteria. Mechanistically, a cell-free factor in the bronchoalveolar lavage fluid contributed to accelerated clearance following passive transfer to naive mice. Further investigation demonstrated increased titres of immunoglobulin A in the bronchoalveolar lavage fluid, but not the blood, of cigarette smoke-exposed mice, including increased titres of NTHi-specific immunoglobulin A, whereas heavy chain joining element (J H ) -/-B-cell-deficient cigarette smoke-exposed mice did not demonstrate decreased bacterial burden following challenge. The present results demonstrate that cigarette smoke exposure results in exacerbated inflammation following challenge with NTHi, as well as increased titres of antibodies that contribute to bacterial clearance.

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Effect of Occupational Exposures on Decline of Lung Function in Early Chronic Obstructive Pulmonary Disease

Abstract: These results suggest a need for secondary prevention by controlling occupational fume exposures.

Cited by 81 publications

References 40 publications

Animal models of chronic obstructive pulmonary disease

Animal models of chronic obstructive pulmonary disease

Copd and occupation: a retrospective cohort study of industrial workers

Mechanisms of clearance of nontypeable Haemophilus influenzae from cigarette smoke-exposed mouse lungs

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