Current Respiratory Medicine Reviews - Volume 8, Issue 6, 2012

Lung cancer (LC) is a highly prevalent malignancy mainly caused by long-term exposure to tobacco smoke, although other substances in the workplace can also cause LC. This paper reviews carcinogens in the workplace linked with occupational LC, including asbestos, radon, silica, nickel, beryllium, chromium and polycyclic aromatic hydrocarbons (PAH). In LC of occupational origin, diagnosis can be difficult due to co-exposure to various carcinogens. The present review is intended to provide additional information that may help in the diagnostic approach and discusses controversial issues on certain substances like silica, beryllium or PAH as etiological factors of LC. Finally, occupational LC preventive measures are discussed.

The health effects of air pollution have been subject to intense study in recent years. These effects have been found in short-term studies, which relate day-to-day variations in air pollution and health, and long-term studies, which have followed cohorts of exposed individuals over time. Epidemiological evidence has concurred with clinical and experimental evidence to correlate current levels of ambient air pollution, both indoors and outdoors, with respiratory effects. The association between ambient air pollution exposure and lung cancer risk indicates that long-term exposure to air pollution may cause lung cancer. In the 1950s evidence of an ongoing epidemic of lung cancer in the United States and Europe led researchers to examine the role of outdoor air pollution, which was considered by some to be a likely cause. This concern is based on the fact that known carcinogens continue to be released into outdoor air from industrial sources, power plants, and motor vehicles. The present article reviews the epidemiologic evidence for this association and discusses the limitations of current studies for estimating the lung cancer risk in the general population. It also identifies research needs and suggests possible approaches to addressing outstanding questions like the causality assessment, which can benefit from biomarker research.

Chronic obstructive pulmonary disease (COPD) is a progressive inflammatory condition of the airways, pulmonary vessels, and lung parenchyma, distinguished by airflow limitation that is not reversible. Cigarette smoking is responsible for the vast majority of COPD, but it does not explain the increasing prevalence worldwide. Occupational and environmental factors have harmful effects on the airway. Particulate pollutants, ozone (O3), and NO2 can all produce deleterious effects on the airways and are increasingly believed to play important roles. As with other conditions, COPD develops due to multiple causes, and genetic factors and the way they relate to environmental factors play an important role. Among these factors, exposure to high levels of ambient air pollution may lead to increased incidence rates of this type of illnesses, and it is also linked to exacerbations of chronic processes. A considerable amount of epidemiological research has been conducted to investigate acute and chronic effects on health resulting from exposure to ambient air pollution, most of it focusing on the health effects of short-term fluctuations in ambient pollution levels. In contrast, evidence is not sufficient to prove a causal relationship between ambient air pollution and COPD. Improving ambient air quality appears to be an effective intervention that could benefit the health of the general population. Determining the role played by retained PM in COPD lung inflammation could lead to novel therapeutic interventions in the future.

Occupational exposures may make a substantive contribution to the etiology of chronic bronchitis, emphysema and airway obstruction. This review critically evaluates the scietific literature to occupational risk factor for COPD.

Different environmental factors can have an effect on the development of asthma, as well as on its clinical expression. The main sources of environmental pollution are the burning of fossil fuels in the combustion engines of different means of transport, in industry and in heating, as well as the biomass used for cooking and heating. Also contributing to this complex mixture is the dust generated by traffic on road surfaces, or substances arising from the degradation of vehicle parts, such as brakes or tires. Among the most abundant components of air pollution in urban areas are particulate matter, nitrogen dioxide, ozone and volatile organic compounds. Sulphur dioxide is particularly abundant in industrial areas. Various mechanisms on how environmental contaminants could cause asthma have been considered. One possibility could be the direct irritation of the airway mucosa. Another possible mechanism could be the combination of the contaminants with various allergens, increasing the allergenic activity. It has also been observed that some environmental contaminants trigger cell inflammation processes. Epigenetic mechanisms, such as hypermethylation of DNA or acetylation of histones, were also described. It has been observed in animal models that a pre-existing mitochondrial dysfunction increases bronchial inflammation after exposure to ragweed pollen extract. In conclusion, it appears that there probably is a harmful effect by environmental contaminants on asthma, increasing both the severity and the prevalence of the disease. But the persistence of some contradictions in the data seems to support the need to continue research in this field, clarifying the magnitude of this effect, as well as the underlying mechanisms, which could help to identify measures to reduce the harmful effects of this exposure.

Data reported in the literature indicate that erythropoietin (EPO) influences mammals respiratory function, for example stimulating pulmonary ventilation. Direct experimentations about possible effects of EPO on respiratory mechanics are lacking. In the present report, the endinflation occlusion method was applied in control and EPO-treated anaesthetised and positive-pressure ventilated rats to assess respiratory mechanics. The method involves a sudden flow arrest after a constant flow inflation, and allows to measure the ohmic airway resistance and the respiratory system elastance. A significant decrement of the ohmic airway resistance after 20 and 30 minutes from i.p. EPO administration was observed in experimental animals, which was not seen in control animals. The elastic characteristics of the respiratory system did not change over time in both groups. Hypothesis about the mechanism(s) explaining the results and potential applications to humans are addressed. In particular, further data were obtained by performing additional experiments suggesting that the observed airway resistance decrement may be related to an EPO-induced increased nitric oxide production, a rather well known bronchodilator agent. Literature and present results indicate that the spontaneous increments of plasmatic EPO concentrations, such as those happening in hypoxia and/or blood loss, may be associated with airway resistance decrement. It is suggested that erythropoietin, beside the well known effect on haematopoiesis, may activate complex physiological responses including haematological, circulatory and respiratory adaptations to hypoxia in mammals.

The prevalence of chronic obstructive pulmonary disease (COPD) is increasing and is now the third most common cause of death in the United States. It is estimated that half of all people in the United States with COPD have not been diagnosed, reflecting factors that include patient delay in seeking help despite symptoms and physician perception that only smoking cessation can improve the course of the disease. Primary care physicians are best placed to identify undiagnosed patients with mild or moderate COPD. Recent evidence from large randomized clinical trials demonstrates that pharmacologic treatments such as tiotropium and salmeterol/fluticasone can benefit patients with mild and moderate COPD, improving lung function, reducing the risk of exacerbations and improving health status. Primary care physicians can help patients and reduce the burden of COPD on healthcare systems by actively assessing patients they suspect may have COPD and treating those diagnosed.

Tuberculosis TB is considered a sobering example of inequity. It is a disease predominantly of the socially and economically disadvantaged. This neglect is evidenced by lack of political support, scarce financial resources for TB programs, and little or no leadership. The emergence and spread of multidrug-resistant tuberculosis (MDR-TB) is threatening global TB control and it represents a major challenge for clinical care and operational management. Worldwide, 3.7% of new cases and 20% of previously treated cases are estimated to have MDR-TB. Unfortunately, since only a quarter of patients with MDR-TB are treated according to established standards and the proportion of treatment success does not exceed 50%, extensively drugresistant tuberculosis (XDR-TB) has already been reported in 84 countries and totally drug resistant cases have been recently described. In most low- and middle-income countries drug sensitivity testing is not performed for new cases or for most patients requiring retreatment. Therefore, patients with underlying drug resistance will receive retreatment with first line drugs and can be predicted to have higher rates of failure and relapse. The development of genotypic methods has generated a genuine revolution in the diagnosis of DR-TB. The polymerase chain reaction allows for the specific identification of M. tuberculosis and the detection of drug resistance in a matter of hours instead of weeks. Unfortunately these techniques are expensive and not available in most high burden countries. Despite the enormous number of cases of TB worldwide, the therapeutic arsenal to treat this disease continues to be very limited, especially for cases with extensive drug resistance. However, for the first time in decades, the pipeline of new anti-TB agents is now growing again inasmuch as new drugs and combination of drugs with interesting potential efficacy to treat TB, MDR-TB and XDR-TB have appeared during the last few years.

Endotracheal tubes (ETT) of intubated patients are constantly challenged with abundant bacteria-laden secretions. These bacteria may rapidly form a well-organized structure, referred to as biofilm, on the inner surface of the ETT. Secretions become very tenacious and are difficult to clear. However, bacteria and secretions can detach spontaneously or become dislodged by suction catheters and enter the lungs, providing a source of infection. Recently, several strategies have been developed to prevent accumulation of mucus and bacterial colonization of the respiratory circuit. In this review, we summarize published studies on antimicrobial ETT-coated and clearance devices. Numerous antimicrobial-impregnated ETTs have been designed with bactericidal/static properties to prevent adhesion of bacteria on ETT surfaces. Several in vitro experiments and animal-studies have shown success in the prevention of bacterial colonization through the use of these specialized ETTs. At present, only two ETT coatings, silver-hydrogel and silver-sulfadiazine in polyurethane, have been tested in clinical trials. Both coatings have been shown to prevent/lower bacterial colonization of the ETT, while only the silver-hydrogel coating decreased bacterial colonization of lungs in a large multicenter study. Another innovative approach is to reduce contaminated-secretions in the ETT-lumen with novel medical devices designed to retrieve accumulated-mucus from the ETT. The mucus shaver and the mucus slurper are two devices intended to reduce loaded-bacteria secretions from within the ETT. While experimental and preliminary clinical trials are promising, there are no large clinical trials showing outcome benefits.