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Chronic exposures to particulate matter with an aerodynamic diameter < 2.5 μm (PM2.5) and ozone pollution can affect respiratory function. ARDS, an often lethal respiratory failure, is most common among older adults. However, few epidemiology studies have investigated an association between air pollution and the risk of ARDS.

Although air pollution is well known to be harmful to the lung and airways, it can also damage most other organ systems of the body. It is estimated that about 500,000 lung cancer deaths and 1.6 million COPD deaths can be attributed to air pollution, but air pollution may also account for 19% of all cardiovascular deaths and 21% of all stroke deaths. Air pollution has been linked to other malignancies, such as bladder cancer and childhood leukemia. Lung development in childhood is stymied with exposure to air pollutants, and poor lung development in children predicts lung impairment in adults. Air pollution is associated with reduced cognitive function and increased risk of dementia. Particulate matter in the air (particulate matter with an aerodynamic diameter < 2.5 μm) is associated with delayed psychomotor development and lower child intelligence. Studies link air pollution with diabetes mellitus prevalence, morbidity, and mortality. Pollution affects the immune system and is associated with allergic rhinitis, allergic sensitization, and autoimmunity. It is also associated with osteoporosis and bone fractures, conjunctivitis, dry eye disease, blepharitis, inflammatory bowel disease, increased intravascular coagulation, and decreased glomerular filtration rate. Atopic and urticarial skin disease, acne, and skin aging are linked to air pollution. Air pollution is controllable and, therefore, many of these adverse health effects can be prevented.

Air pollution exposure is associated with acute exacerbation, disease progression, and mortality in patients with idiopathic pulmonary fibrosis (IPF). The objective of this study was to describe the impact of air pollution exposures on disease severity, as well as changes in lung function, in patients with IPF.

Air pollution exposure is a well-established risk factor for several adverse respiratory outcomes, including airways diseases and lung cancer. Few studies have investigated the relationship between air pollution and interstitial lung disease (ILD) despite many forms of ILD arising from environmental exposures. There are potential mechanisms by which air pollution could cause, exacerbate, or accelerate the progression of certain forms of ILD via pulmonary and systemic inflammation as well as oxidative stress. This article will review the current epidemiologic and translational data supporting the plausibility of this relationship and propose a new conceptual framework for characterizing novel environmental risk factors for these forms of lung disease.

Household air pollution (HAP) from biomass fuels, coal, and kerosene burned in open fires, primitive stoves, and lamps causes at least 2 million deaths per year. Many of these deaths occur in children <5 years of age with pneumonia and in women with COPD, lung cancer, and cardiovascular disease. HAP is inextricably linked to poverty, with activities to obtain fuel consuming a large proportion of the time and financial resources of poor households. Thus, fewer resources used in this way means less is available for basic needs like food, education, and health care. The burden of work and the exposure to smoke, particularly during cooking, are predominantly borne by women and children. Although historically HAP has not received sufficient attention from the scientific, medical, public health, development, and policy-making communities, the tide has clearly changed with the broad-based support and launch of the Global Alliance for Clean Cookstoves in 2010. There is now considerable reason for optimism that this substantial cause of cardiorespiratory morbidity and mortality will be addressed comprehensively and definitively. Drawing on our experience from four continents, we provide background information on the problem of HAP, health impacts of HAP, opportunities for research, and the current best solutions.

The diagnosis of and criteria for the evaluation of asbestos-related disease impairment remains controversial after decades of research. Assessing agreement among experts who study pneumoconiosis, and diagnose and treat patients with asbestos-related respiratory conditions may be the first step in clarifying clinical and forensic/administrative issues associated with asbestos-related pulmonary conditions.

A previous American College of Chest Physicians Consensus Statement on asthma in the workplace was published in 1995. The current Consensus Statement updates the previous one based on additional research that has been published since then, including findings relevant to preventive measures and work-exacerbated asthma (WEA).

Neutrophilic airway inflammation, as defined by cell counts in respiratory tract lining fluid (RTLF), is a key end point in many studies of respiratory toxicity in both healthy and asthmatic subjects. BAL and sputum induction (SI) are the most common methods of sampling RTLF in such studies. However, the comparability of these methods (BAL and SI) after experimental treatment has not been investigated in a head-to-head controlled trial.

To develop a comprehensive disease-specific COPD severity instrument for survey-based epidemiologic research.

Controlled human exposure studies have produced conflicting results regarding the effect of ozone on the early bronchoconstrictor response to inhaled allergen in specifically sensitized asthmatic subjects. Spirometric parameters do not necessarily reflect the airway inflammatory effects of inhaled ozone or allergen.

Laboratory-based spirometry is the “gold standard” for the assessment of lung function, both in clinical and research protocols. These spirometers, however, are neither practical nor affordable for home-based monitoring or studies that collect data in multiple locations. Traditionally, peak flowmeters have been used, but they have important limitations.

To compare the expression of plasminogen activators (PA) and plasminogen activator inhibitors (PAI) in normal lung mucosa and lung carcinomas.

Sixteen consecutive patients with one or more osteolytic bone lesions of the chest wall radiologically confirmed underwent ultrasonically guided aspiration biopsy. Nine patients (56.2 percent) had bronchogenic carcinoma with a direct extension. Other diagnostic techniques had failed to diagnose disease in these patients. The lesion showed heterogeneous echogenicity (n = 16) caused by the hyperechoic signals of bone fragments. The interruption of the cortex bone was detected in all cases and extraosseous tumor portion in 14 of 16 patients (87.5 percent). No respiratory motions of the lesion could be demonstrated (n = 16). Definitive histologic diagnosis was made in 14 of the 16 patients (87.5 percent). In malignancy, diagnosis was established in 13 of 14 patients (92.8 percent). Of two confirmed benign lesions, one diagnosis of tuberculosis was obtained. No complication occurred. Sonography and consequently ultrasonically guided aspiration biopsy are a useful, accurate, safe, and low-cost technique for osteolytic lesions in thoracic diseases.

To evaluate the validity of a state-of-the-art computerized planimetry technique for estimation of total lung capacity (TLC) from chest radiographs, when applied to patients with clinical lung disease receiving routine chest radiographs.

Since parenteral β2-adrenergic stimulation can induce hypokalemia, we postulated that administration of β2adrenoreceptor agonists by inhalation could induce the same. We administered the usual clinical doses of three commonly used bronchodilators to each of six subjects receiving assisted mechanical ventilation in line with the ventilator: two β2-adrenoreceptor agonists, metaproterenol, 5 percent solution, and isoetharine, 1 percent solution; and the anticholinergic agent atropine as a control. Each bronchodilator was nebulized over 10 to 15 minutes in random order, four hours apart, and given to every subject. Plasma potassium was measured at five-minute intervals and arterial blood gases at 15-minute intervals, for a total of 50 minutes after administration of each bronchodilator. Following administration of each drug, plasma potassium showed an average decline. The mean decline in plasma potassium from baseline was statistically significant for metaproterenol (p = 0.04) and atropine (p = 0.001) but not for isoetharine (p=0.09). Although there were no statistically significant differences among the declines in plasma potassium induced by the three drugs, metaproterenol caused the greatest decline (–0.6 mEq/L). (Chest 1988; 94:763-66)

Controlled human exposure studies have suggested that the National Ambient Air Quality Standard for ozone (O3) may not provide a margin of safety to protect the most susceptible members of the population from adverse health effects. Although the subgroups of the population that are most susceptible to O3have not been identified, recent work in our laboratory suggested that methacholine responsiveness might be an important determinant of susceptibility to O3. Patients and methods: To test the hypothesis that methacholine responsiveness is correlated with FEV1response after O3exposure, we conducted methacholine challenge tests and O3(0.20 ppm) and filtered air exposures for 4 h with moderate exercise on 66 healthy individuals.

Study objective: To estimate the incidence of respiratory symptoms and physiologic abnormalities after inhalation of common irritant chemicals.

The proposed NIOSH surveillance case definition is likely to miss many cases of work-related asthma because of its relatively stringent requirements for information that is not routinely collected by primary case providers. As the case definition is implemented in the SENSOR program, further research should address the sensitivity, specificity, and validity of the various requirements of the case definition. Efforts will also need to be made to educate the clinician population who will be reporting cases, as the success of the program will depend on adequate data collection by the diagnosing physician.

Studies investigating the relation between respiratory symptoms and change in ventilatory function have been limited by use of reported symptoms at a single point in time. To assess the relation between the longitudinal pattern of reported cough, phlegm, wheeze, and dyspnea and ventilatory loss, we prospectively investigated changes in FVC and FEV1associated with development, resolution, or persistence of these symptoms over a 3- to 5-year period in 446 asbestos-exposed workers. Longitudinally reported symptoms changed frequently, with 52 to 61% of subjects reporting a specific symptom noting resolution or development of that symptom during follow-up. Initially reported symptoms were not predictive of accelerated loss of FVC or FEV1. In contrast, development of any new respiratory symptom, and to a lesser extent persistence of symptoms during follow-up, were associated with significantly greater ventilatory losses compared with asymptomatic individuals, ranging from 28 mL/yr in FEV1for newly developed dyspnea, to 67 mL/yr in FVC for developed wheeze (p<0.01). We conclude that development or persistence of respiratory symptoms over time, rather than the presence of symptoms per se, is predictive of future ventilatory loss. Recognition of interval changes in symptom reporting during surveillance of asbestos-exposed workers may effectively identify groups at risk for progressive ventilatory impairment.

Study objective: To report the occurrence of persistent respiratory disorders, including irritant-induced asthma, among adults living and working near an environmental spill of the pesticide, metam sodium, after the derailment of a tank car.

This study describes the extent of agreement in classification of chest radiographs using the International Labor Organization (ILO) classification among six readers from the United States and Canada. A set of 119 radiographs was created and read by three Canadian and three US readers. The two ratings of interest were profusion (scored from 0/-to 3/+) and pleural abnormalities consistent with pneumoconiosis (scored with the ILO system, then collapsed into a yes/no). We used a number of approaches to evaluate interreader agreement on profusion and pleural changes, determining concordance, observed agreement, kappa statistic, and a new measure to approximate sensitivity and specificity. This study found that five of six readers had good fair to good agreement for pleural findings and for profusion as a dichotomous variable (≥ 1/0 vs ≤ 0/1) using the kappa statistic, while a sixth reader had poor agreement. We found that concordance, expressed as percent agreement, was higher for normal radiographs than for ones that showed disease, and describe the use of the kappa statistic to control for this finding. This analysis adds to the existing literature with the use of the kappa statistic, and by presenting a new measure for “underreading” and “overreading” tendencies.

Ultrasound results for 11 patients with HPN confirmed by CXR were compared with those for 100 healthy subjects. The observation of the hyperechogenic line of the pleuropulmonary surface (normal subjects) showed back-and-forth respiratory movements in every case which we call the “gliding sign.” Ultrasonographic signs were shown in all patients with HPN. Visualizing the gassy effusion above the pleural fluid, the disappearance of the “gliding sign” (n = 11) indicates PN. The image of the HPN allows in addition a “curtain sign” which depicts the movement of air/fluid level (n= 11), the pulmonary collapse being calculated across the liquid window whose echostructure is analyzed. A “polymicrobullous” image (n = 2) caused by air microbubbles within the fluid effusion, is reported. We conclude that echography appears to be a new approach to diagnosing HPN, which is particularly useful during or after ultrasonically guided procedures including pleural drainage, and should be recognized by sonographers.

Ozone effects on lung function are particularly important to understand in the context of the air pollution-health outcomes epidemiological literature given the complex relationships between ozone and other air pollutants with known lung function effects.

The effect of interstitial pulmonary fibrosis on pregnancy is unclear. We present the findings in a 31-year-old woman with severe pulmonary fibrosis (vital capacity, 37 percent of predicted) secondary to hard metal disease who went through a successful term pregnancy. The patient was a grinder of tungsten-carbide drill bits who developed pneumonitis and subsequent fibrosis. Her therapy required steroids and cyclophosphamide for stabilization of her pulmonary function prior to her pregnancy. At six months' gestation, right heart catheterization showed normal cardiac output and pulmonary arterial and wedge pressures. Stage 2 exercise study demonstrated a maximum oxygen consumption of 1.17 L/min (53 percent of predicted). The patient was able to exercise to a maximum workload of 300 kpm/min (32 percent of predicted). She became hypoxemic (arterial oxygen pressure, 54 mm Hg) at 150 kpm/min. Her pregnancy concluded with an uncomplicated normal vaginal delivery requiring only supplemental oxygen and spinal anesthesia. Review of the few similar cases suggests that a woman can have a successful pregnancy despite severe pulmonary dysfunction.

A 34-year-old chemical manufacturing worker had new onset of work-related asthma after several years of exposure to the fungicide, captafol. On specific bronchial challenge testing, he demonstrated a marked and persistent fall in FEV1. Cessation of exposure resulted in improved symptoms and pulmonary function. The delay in symptoms after several years of workplace exposure and the dual reaction demonstrated on specific bronchial challenge testing suggest sensitization to some component of technical-grade captafol, but an IgE response was not detected.

We report two cases of pneumothorax detected by echographic examination immediately after ultrasonically guided aspiration biopsy and confirmed by chest x-ray film. The pneumothorax was characterized by the disappearance of the lung tumor. In the real-time image, the respiratory excursions of the visceral pleura also disappeared.