Human health effects of air pollution

Background: Pulmonary rehabilitation is recognized as a core component of the management of individuals with chronic respiratory disease. Since the 2006 American Thoracic Society (ATS)/European Respiratory Society (ERS) Statement on Pulmonary Rehabilitation, there has been considerable growth in our knowledge of its efficacy and scope.

Purpose: The purpose of this Statement is to update the 2006 document, including a new definition of pulmonary rehabilitation and highlighting key concepts and major advances in the field.

Methods: A multidisciplinary committee of experts representing the ATS Pulmonary Rehabilitation Assembly and the ERS Scientific Group 01.02, “Rehabilitation and Chronic Care,” determined the overall scope of this update through group consensus. Focused literature reviews in key topic areas were conducted by committee members with relevant clinical and scientific expertise. The final content of this Statement was agreed on by all members.

Results: An updated definition of pulmonary rehabilitation is proposed. New data are presented on the science and application of pulmonary rehabilitation, including its effectiveness in acutely ill individuals with chronic obstructive pulmonary disease, and in individuals with other chronic respiratory diseases. The important role of pulmonary rehabilitation in chronic disease management is highlighted. In addition, the role of health behavior change in optimizing and maintaining benefits is discussed.

Conclusions: The considerable growth in the science and application of pulmonary rehabilitation since 2006 adds further support for its efficacy in a wide range of individuals with chronic respiratory disease

Read More: http://www.atsjournals.org/doi/abs/10.1164/rccm.201309-1634ST

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An official American thoracic society/European respiratory society statement: Key concepts and advances in pulmonary rehabilitation

Air pollution is a heterogeneous, complex mixture of gases, liquids, and particulate matter. Epidemiological studies have demonstrated a consistent increased risk for cardiovascular events in relation to both short- and long-term exposure to present-day concentrations of ambient particulate matter. Several plausible mechanistic pathways have been described, including enhanced coagulation/thrombosis, a propensity for arrhythmias, acute arterial vasoconstriction, systemic inflammatory responses, and the chronic promotion of atherosclerosis. The purpose of this statement is to provide healthcare professionals and regulatory agencies with a comprehensive review of the literature on air pollution and cardiovascular disease. In addition, the implications of these findings in relation to public health and regulatory policies are addressed. Practical recommendations for healthcare providers and their patients are outlined. In the final section, suggestions for future research are made to address a number of remaining scientific questions.

https://cdr.lib.unc.edu/downloads/n870zt13s

Air Pollution and Cardiovascular Disease A Statement for Healthcare Professionals From the Expert Panel on Population and Prevention Science of the American Heart Association

Lung function testing: selection of reference values and interpretative strategies.

INTRODUCTION Herein is the discussion of the 2006 A&WMA Critical Review1,2 on “Health Effects of Fine Particulate Air Pollution: Lines that Connect.” In the review, Drs. C. Arden Pope III and Douglas Dockery addressed the epidemiological evidence for the effects of particulate matter (PM) on human health indicators. The review documents substantial progress since the 1997 Critical Review3 in the areas of: (1) short-term exposure and mortality; (2) long-term exposure and mortality; (3) time scales of exposure; (4) the shape of the concentration-response function; (5) cardiovascular disease; and (6) biological plausibility. Invited and contributing discussants agree and disagree with points made in the review. Each discussion is self-contained and adds information relevant to the topic. Joint authorship of this article does not imply that a discussant subscribes to the opinions expressed by others. Commentaries are the opinions of the author only and do not necessarily reflect the positions of their respective organizations. In particular, Dr. Costa’s comments have not been reviewed by U.S. Environmental Protection Agency (EPA) and do not reflect official positions or policies of the agency. CRITICAL REVIEW DISCUSSION ISSN 1047-3289 J. Air & Waste Manage. Assoc. 56:1368–1380

Health effects of fine particulate air pollution: line that connect

This paper outlines the history of air pollution in the UK, describes the types of pollutant now in the atmosphere, and discusses the relation between air pollution and health. The primary pollutants, which are directly discharged into the atmosphere, often from vehicle exhaust emissions, are: (1) sulphur dioxide (SO2); (2) nitrogen oxides (NOx); (3) smoke and particulates; (4) carbon monoxide (CO); (5) carbon dioxide (CO2); (6) organic compounds; and (7) metals, especially lead and calcium. The secondary pollutants, derived from primary pollutants, by chemical changes, include: (1) ground ozone, an important constituent of photochemical smog; and (2) acid aerosols. It is now proved beyond reasonable doubt that sufficiently high concentrations of atmospheric pollution have severe health effects. Various biological and medical methodologies can be used to evaluate their effects on health. Asthma and rhinitis are two important respiratory diseases, whose causes include air pollution. For the covering abstract see IRRD 869702.

Air pollution and health

The diaphragm is normally the main inspiratory muscle and diaphragm strength in chronic obstructive pulmonary disease (COPD) is therefore of interest. We assessed diaphragm strength in 20 patients with severe stable COPD (mean FEV1 0.61, mean thoracic gas volume [Vtg] 5.31) and seven normal control subjects, measuring both maximal sniff transdiaphragmatic pressure (sniff Pdi(max)) and twitch transdiaphragmatic pressure (Tw Pdi) elicited by cervical magnetic stimulation (CMS) of the phrenic nerve roots at FRC. Acute-on-chronic hyperinflation was examined in four patients. Mean Tw Pdi in patients and control subjects was 18.5 cm H2O and 25.4 cm H2O, respectively (p < 0.01), and mean sniff Pdi was 81.9 cm H2O and 118 cm H2O, respectively (p < 0.001). Reduction in mean intrathoracic pressures was more marked; twitch esophageal pressure (Tw Pes) was -7.3 cm H2O and -16.3 cm H2O, respectively (p < 0.001) and sniff Pes was -67 cm H2O and -97.8 cm H2O (p < 0.001). During acute-on-chronic hyperinflation there was a linear negative correlation of Tw Pdi with increasing lung volume of 3.5 cm H2O/L. The ability of the diaphragm to generate transdiaphragmatic, and particularly a negative intrathoracic, pressure is reduced in COPD and these changes are exaggerated with acute-on-chronic hyperinflation.

Diaphragm strength in chronic obstructive pulmonary disease.

Why must the chest physician become familiar with assessment of the respiratory muscles? Firstly, because dyspnoea in patients in whom no pulmonary cause can be detected may be due to respiratory muscle weakness.t2 Even moderately severe muscle weakness may be difficult to detect clinically3 and, indeed, it is possible to have total paralysis of the diaphragm without life threatening consequences.4 Secondly, because patients with clearly documented generalised neuromuscular disease usually also have respiratory muscle weakness2 and, for selected cases, treatment in the form of non-invasive ventilation is indicated.5 Finally, there has recently been increased awareness that respiratory muscle weakness can be a compounding factor in other disease processes such as malnutrition6 and steroid therapy.7 For all of these reasons it is important for respiratory physicians to initiate and to be able to interpret simple tests ofrespiratory muscle function. For most patients the suspicion of clinically important respiratory muscle weakness may be confirmed or excluded by simple tests that can be performed in the general hospital setting without the purchase of expensive equipment, but in some patients complex tests in a specialised laboratory are necessary (fig 1). In this editorial the current techniques to assess respiratory muscle strength are reviewed with

https://thorax.bmj.com/content/thoraxjnl/50/11/1131.full.pdf

Measurement of respiratory muscle strength.

In a study of 147 subjects (50 normals, 50 with obstructive, and 47 with restrictive lung function), the mean reduction in forced vital capacity from standing to supine (delta FVC) was 7.5% (SD +/- 5.7), 11.2% (+/- 13.4), and 8.2% (+/- 7.7) respectively, with no significant difference between groups. The respective 95% upper confidence limits were 19%, 38% and 24%. We conclude that delta FVC greater than 25% associated with normal or restrictive lung function or greater than 35% associated with airways obstruction should be an indication for further study of diaphragm function.

Fall in vital capacity with posture

Thirty patients with breathlessness and diaphragm weakness were studied by measuring transdiaphragmatic pressures during maximal inspirations to total lung capacity, maximal static inspiratory efforts from residual volume, and maximal sniffs from functional residual capacity Maximal static respiratory mouth pressures were also recorded, and rib cage and abdominal movements were monitored with pairs of magnetometers Sniff transdiaphragmatic pressure was abnormally low in all patients and was correlated with transdiaphragmatic pressure during other maneuvers, and with maximal static inspiratory mouth pressures There was no relationship between the severity of dyspnea and transdiaphragmatic pressure in the group as a whole The weakest patients had orthopnea and paradoxical inward inspiratory motion of the anterior abdominal wall; measurements suggested that at least 30 cm H2O transdiaphragmatic pressure was required to overcome the hydrostatic pressure of the abdominal contents By contrast, patients wit

Malcolm Green

Papers

Air pollution and health

Diaphragm strength in chronic obstructive pulmonary disease.

Measurement of respiratory muscle strength.

Fall in vital capacity with posture

Assessment of Diaphragm Weakness