Books on the topic 'Reduced airgap'

Heart function and sleep are closely associated. While NREM sleep reduces cardiac workload, phasic REM sleep increases sympathetic activity and cardiac vulnerability. Heart failure (HF) patients suffer from disturbed sleep due to frequent awakenings, periodic limb movements, sleep apnea, and depression. Insomnia seems to be associated with incident HF, and, when comorbid, results in a vicious circle. There is much evidence of a relationship between breathing disturbances during sleep and heart diseases. At least 50% of HF patients suffer from obstructive (OSA) or central (CSA) sleep apnea, both associated with impaired prognosis. OSA is a risk factor for arterial hypertension, atrial fibrillation, and HF. Continuous positive airway pressure devices reduce adverse cardiac events and improve outcome in severe OSA in compliant subjects. Adaptive servoventilation (ASV) is superior to other therapeutic options for CSA. However, the use of ASV is contraindicated in severe HF with reduced, but not preserved, ejection fraction.

The difficult airway invariably presents itself to all airway managers and is mostly unpredictable in the context of rapid response team (RRT) calls. A multiprofessional difficult airway team (DAT) that could be called for airway emergencies is likely to reduce complications and death. The DAT is organized with predefined roles for each member so that rapid intervention occurs during the emergency. Priority is given to oxygenation throughout the airway response. The anticipated and unanticipated difficult airways should be approached differently and often require medication adjuncts that should be carefully chosen. Airway devices such as the video laryngoscope and the laryngeal mask airway (LMA) have dramatically improved the ability to secure an airway quickly. Finally, it is important to recognize when a surgical airway is needed in the setting of the RRT calls.

This chapter describes positive airway pressure (PAP) therapy for sleep disordered breathing. Continuous PAP (CPAP) acts as a mechanical splint on the upper airway and is the treatment of choice for moderate to severe obstructive sleep apnea (OSA). Autotitrating CPAP may be used when the pressure demand for stabilizing the upper airway is quite variable. In other cases, fixed CPAP is sufficient. There is robust evidence that CPAP reduces the symptomatic burden and risk of cardiovascular comorbidity in patients with moderate to severe OSA. Bilevel PAP is indicated for treatment of respiratory diseases characterized by chronic alveolar hypoventilation, which typically deteriorates during sleep. Adaptive servo-ventilation is a mode of bilevel PAP used to treat Cheyne–Stokes respiration with central sleep apnea . It is crucial that caregivers help patients get used to and be compliant with PAP therapy. Education, support, and resolution of adverse effects are mandatory for therapeutic success.

Failed or difficult intubation is still a major cause of maternal morbidity and mortality. The management of the airway in the pregnant patient requires careful consideration of anatomical and physiological changes, training issues, and situational factors. Despite significant improvements in monitoring and airway equipment, and a reduction in anaesthetic-related maternal mortality, the incidence of failed intubation in the pregnant woman in many units has remained between 1/250 and 1/300. This may result from many factors such as the reduction of the number of caesarean deliveries performed under general anaesthesia which has resulted in limited opportunities to teach airway skills in obstetrics, the increased incidence of obesity, and the rise in maternal age and associated co-morbidities. Improved training and careful planning and performance of a general anaesthetic (i.e. reducing the risk of aspiration; optimum pre-oxygenation, patient positioning, and application of cricoid pressure; and availability of appropriate airway equipment) have the potential to reduce airway-related morbidity and mortality in the pregnant woman. Simple bedside tests such as Mallampati scoring, thyromental distance, neck movement, and ability to protrude the mandible may help to predict a potential difficult airway, particularly when used in combination. Management of a predicted difficult airway requires early referral to the anaesthetists, formulation of an airway management strategy, and involvement of the multidisciplinary team in decision-making. Fibreoptic equipment and skills should be readily available when required. Management of the unpredicted difficult airway should make maintenance of maternal and fetal oxygenation the primary goal. Decision-making during a failed intubation on whether to proceed or wake the patient should involve the obstetrician and ideally be planned in advance. The periods during extubation and recovery are high risk and require preparation and planning in advance.

Retention of airway mucus is one of the major problem that confronts post-operative and critically-ill patients, as well as the caregivers that address it. Retained secretions increase the work of breathing and promote hypoxaemia, atelectasis, and pneumonia. The airway-intubated patient is at particular risk of retaining mucus, as the presence of the tube interrupts normal flow of airway secretions toward the larynx by the mucociliary escalator and coughing effectiveness is degraded by a glottis that is stented open and cannot close effectively. Clearance of mucus is aided by using sufficient gas stream and total body hydration to reduce sputum viscosity and lubricate secretion plugs. Airway suctioning, a routine, but inherently traumatic experience for the patient, may clear the central airway, but leave peripheral airways unrelieved of their secretion burden. Prone positioning appears to confer an advantage regarding secretion drainage and clearance. Physiotherapy techniques may be useful in re-establishing and maintaining airway patency.

During positive pressure ventilation the lung volume is reduced because of loss of respiratory muscle tone. This promotes airway closure that occurs in dependent lung regions. Gas absorption behind the closed airway results sooner or later in atelectasis depending on the inspired oxygen concentration. The elevated airway and alveolar pressures squeeze blood flow down the lung so that a ventilation/perfusion mismatch ensues with more ventilation going to the upper lung regions and more perfusion going to the lower, dependent lung. Positive pressure ventilation may impede the return of venous blood to the thorax and right heart. This raises venous pressure, causing an increase in systemic capillary pressure with increased capillary leakage and possible oedema formation in peripheral organs. Steps that can be taken to counter the negative effects of mechanical ventilation include an increase in lung volume by recruitment of collapsed lung and an appropriate positive end-expiratory pressure, to keep aerated lung open and to prevent cyclic airway closure. Maintaining normo- or hypervolaemia to make the pulmonary circulation less vulnerable to increased airway and alveolar pressures, and preserving or mimicking spontaneous breaths, in addition to the mechanical breaths, since they may improve matching of ventilation and blood flow, may increase venous return and decrease systemic organ oedema formation (however, risk of respiratory muscle fatigue, and even overexpansion of lung if uncontrolled).

Beside reduction in tidal volume limiting peak airway pressure minimizes the risk for ventilator-associated-lung-injury in patients with acute respiratory distress syndrome. Pressure-controlled, time-cycled ventilation (PCV) enables the physician to keep airway pressures under strict limits by presetting inspiratory and expiratory pressures, and cycle times. PCV results in a square-waved airway pressure and a decelerating inspiratory gas flow holding the alveoli inflated for the preset time. Preset pressures and cycle times, and respiratory system mechanics affect alveolar and intrinsic positive end-expiratory (PEEPi) pressures, tidal volume, total minute, and alveolar ventilation. When compared with flow-controlled, time-cycled (‘volume-controlled’) ventilation, PCV results in reduced peak airway pressures, but higher mean airway. Homogeneity of regional peak alveolar pressure distribution within the lung is improved. However, no consistent data exist, showing PCV to improve patient outcome. During inverse ratio ventilation (IRV) elongation of inspiratory time increases mean airway pressure and enables full lung inflation, whereas shortening expiratory time causes incomplete lung emptying and increased PEEPi. Both mechanisms increase mean alveolar and transpulmonary pressures, and may thereby improve lung recruitment and gas exchange. However, when compared with conventional mechanical ventilation using an increased external PEEP to reach the same magnitude of total PEEP as that produced intrinsically by IRV, IRV has no advantage. Airway pressure release ventilation (APRV) provides a PCV-like squared pressure pattern by time-cycled switches between two continuous positive airway pressure levels, while allowing unrestricted spontaneous breathing in any ventilatory phase. Maintaining spontaneous breathing with APRV is associated with recruitment and improved ventilation of dependent lung areas, improved ventilation-perfusion matching, cardiac output, oxygenation, and oxygen delivery, whereas need for sedation, vasopressors, and inotropic agents and duration of ventilator support decreases.

Continuous positive airways pressure (CPAP) is a mechanical ventilation (MV) mode in which the patient breaths spontaneously at a higher than atmospheric pressure. CPAP increases transpulmonary pressure inducing an FRC increase and a WOB decrease in acute restrictive lung pathology, with improvement of gas exchange. The work of breathing (WOB) is also reduced in the resistive component and inspiratory effort can be reduced if the patient experiences airway collapse and flow limitation, where CPAP counteracts the inspiratory threshold load represented by intrinsic PEEP. CPAP has been proven to be useful in many clinical situation and the technique for administration has a pivotal role in clinical efficacy of the technique. It’s crucial to keep the positive pressure as constant as possible and to avoid any technical increase of WOB. These goals can be achieved by continuous or demand flow systems. The modern ventilators work well and have overcome the valve function problem, which made difficult to use CPAP with old-generation machines.

Cystic fibrosis (CF) is a genetic disease resulting in an impaired mucociliary clearance, chronic bacterial airway infection, and inflammation. The progressive destruction of the lungs is the main cause of morbidity and premature death. Diverse other organ systems such as heart, muscles, bones, gastro-intestinal tract, and sweat glands are often also affected and interfere with exercise capacity. Hence, exercise capacity is reduced as the disease progresses mainly due to reduced functioning of the muscles, heart, and/or lungs. Although there is still growing evidence of positive effects of exercise training in CF on exercise capacity, decline of pulmonary function, and health-related quality of life, the observed effects are encouraging and exercise should be implemented in all patient care. More research is needed to understand pathophysiological mechanisms of exercise limitations and to find optimal exercise modalities to slow down disease progression, predict long-term adherence, and improve health-related quality of life.

During emergency cesarean delivery (CD), indicated by immediate threat to fetal or maternal life, the anesthesiologist must quickly provide anesthesia that is rapid in onset and safe for both patients. Neuraxial anesthesia using well-functioning in-dwelling epidural catheters is achievable with early enough notification. Still, general anesthesia is often the most expedient method. Advanced airway devices and evolving difficult airway management algorithms have likely contributed to observed reductions maternal morbidity and mortality associated with general anesthesia. Long before the crisis arises, other measures can mitigate against risk, including early assessment and identification of at-risk patients, establishment of effective neuraxial labor analgesia in high-risk patients, and effective teamwork and communication. Establishing interprofessional labor and delivery unit goals and strategies, conducting team debrief sessions after each STAT CD, and identifying obstacles and generating case-specific strategies to overcome them constitute a resource-effective way to substantially reduce decision-to-delivery intervals and improve neonatal outcomes.

Epidermolysis bullosa (EB) is a genetic skin disorder with multiple modes of inheritance that causes blister formation from shear injury and results in extensive scarring. Children with EB provide an array of unique challenges when presenting for anesthetic care. Anticipation and management of a potentially difficult airway as well as the protection of fragile skin and mucous membranes are high priorities during anesthetic planning. Complications can arise with use of even the most routine anesthesia monitors and placement of a simple peripheral IV line. Thorough preoperative planning and meticulous perioperative care will reduce complications and result in a smooth anesthetic for both patient and clinician.

General anaesthesia (GA) is most often indicated for category 1 (immediate threat to life of mother or baby) caesarean delivery (CD) or when neuraxial anaesthesia has failed or is contraindicated. Secure intravenous access is essential. Jugular venous cannulation (with ultrasound guidance) is required if peripheral access is inadequate. A World Health Organization surgical safety checklist must be used. The shoulders and upper back should be ramped. Left lateral table tilt or other means of uterine displacement are essential to minimize aortocaval compression, and a head-up position is recommended to improve the efficiency of preoxygenation and reduce the likelihood of gastric contents reaching the oropharynx. Cricoid pressure is controversial. In the United Kingdom, thiopental remains the induction agent of choice, although there is scant evidence upon which to avoid propofol. In pre-eclampsia, it is essential to obtund the pressor response to laryngoscopy with remifentanil or alfentanil. Rocuronium is an acceptable alternative to succinylcholine for neuromuscular blockade. Sugammadex offers the possibility of swifter reversal of rocuronium than spontaneous recovery from succinylcholine. Management of difficult tracheal intubation is focused on ‘oxygenation without aspiration’ and prevention of airway trauma. The Classic™ laryngeal mask airway is the most commonly used rescue airway in the United Kingdom. There is a large set of data from fasted women of low body mass index who have undergone elective CD safely with a Proseal™ or Supreme™ laryngeal mask airway. Sevoflurane is the most popular volatile agent for maintenance of GA. The role of electroencephalography-based depth of anaesthesia monitors at CD remains to be established. Intraoperative end-tidal carbon dioxide tension should be maintained below 4.0 kPa.

This chapter summarizes data on sleep–wake disturbances in humans at high altitude and in space. High altitude exposure is associated with periodic breathing and a trend toward reduced slow-wave sleep and sleep efficiency in healthy individuals. Some subjects are affected by altitude-related illness (eg, acute and chronic mountain sickness, high-altitude cerebral and pulmonary edema). Several drugs are available to prevent and treat these conditions. Data about the effects of microgravity on sleep are limited and do not allow the drawing of firm conclusions. Microgravity and physical and psychological factors are responsible for sleep–wake disturbances during space travel. Space missions are associated with sleep restriction and disruption and circadian rhythm disturbances encouraging use of sleep medication. An unexplained and unexpected finding is the improvement in upper airway obstructive breathing events and snoring during space flight.

Inhalation injury represents one of the most serious associated injuries complicating the care of thermally-injured patient. It can result in severe respiratory failure and acute respiratory distress syndrome (ARDS) by three mechanisms—thermal or chemical injury, and impairment of systemic oxygen supply. Thermal injury can cause erythema, ulceration, and progressive, life-threatening oedema, particularly of the upper airways. Chemical injury is due to irritants or cytotoxic compounds, and depends on the material burned, the temperature of the fire, and the amount of oxygen present in the fire environment. It is responsible for irritation, ulceration, and oedema of the mucosal surface, and the initiation of a lung inflammatory reaction when small particles reach the alveoli. Moreover, the increased vascular permeability, and the reduced surfactant production carry a significant risk in the development of pneumonia and ARDS. Bronchospasm and upper airway oedema can occur rapidly, while lower airway oedema can be asymptomatic for up to 24 hours. Lung imaging techniques may not reveal injured areas for the first 24–48 hours. Fibre optic bronchoscopy is considered to be the most direct diagnostic method for the definitive diagnosis of inhalation injury. The patient management includes airways assessment, adequate fluid resuscitation, and mechanical ventilation when required. All victims of smoke inhalation should be always evaluated for cyanide and carbon monoxide poisoning.

This chapter provides a comprehensive update on the prevention, recognition, and treatment of low bone mineral density in people with CF. As life expectancy improves, the extra-pulmonary complications of CF are becoming increasingly important to quality of life. Up to 25 per cent of CF patients have reduced bone mineral density in adulthood, leading to the development of fragility fractures which cause pain, thereby interfering with airway clearance and predisposing to pulmonary infection. Osteoporosis can be a relative contraindication for lung transplantation. Other important musculoskeletal issues including CF arthropathy, growth, and urinary incontinence are covered. CF arthropathy is a non-erosive episodic sero-negative arthritis, often difficult to treat and which may require specialist input. Urinary incontinence is common girls and women with CF and has a negative impact on quality of life and ability to complete therapies. The pathophysiology and management of urinary incontinence are discussed.

Day-stay surgery is becoming increasingly common the world over. There are several benefits of avoiding in-hospital care. Early ambulation reduces the risk for thromboembolic events, facilitates wound healing, and avoiding admission reduces the risk for hospital-related infection. Additionally, the risk of neurocognitive side-effects can be avoided by returning the elderly patient to their home environment. Day-stay anaesthesia calls for adequate and structured preoperative assessment and patient evaluation, and the potential risk associated with surgery and anaesthesia should be assessed on an individual basis. Need for preoperative testing should be based on functional status of the patient and preoperative medical history but even the surgical procedure should be taken into account. Preoperative fasting should be in accordance with modern guidelines, refraining from food for 6 hours and fluids for 2 hours prior to induction in low-risk patients. Preventive analgesia and prophylaxis of postoperative nausea and vomiting (PONV) should be administered preoperatively. Local anaesthesia should be administered prior to incision, constituting part of multimodal analgesia. The multimodal analgesia strategy should also include paracetamol and a non-steroidal anti-inflammatory drug in order to reduce the noxious stimulus from the surgical field. Third-generation inhaled anaesthetics or a propofol-based maintenance are both feasible alternatives. Titrating depth of anaesthesia by using an EEG-based depth of anaesthesia monitor may facilitate the recovery process. The laryngeal mask airway has become commonly used and has several advantages. Ultrasound-guided peripheral blocks may facilitate the early postoperative course by reducing pain and avoiding the use of opiates. Perineural catheters may be an option for prolongation of the block following painful orthopaedic procedures but a strict protocol and follow-up must be secured. Not only pain but even nausea and vomiting should be prevented, and therefore risk stratification, for example by the Apfel score, and PONV prophylaxis in accordance with the risk score is strongly recommended. Early ambulation should be encouraged postoperatively. Safe discharge should include an escort who also remains at home during the first postoperative night. Analgesics should be provided and be readily available for self-care when the patient comes home. Pain medication should include an opioid; however, the benefit versus risk must be assessed on an individual basis. Patients should also be instructed about a rescue return-to-hospital plan. Quality of care should include follow-up and analysis of clinical practice, and institution of methods to improve quality should be enforced for the benefit of the ambulatory surgical patient.

Mechanical ventilation is an efficacious therapy to respiratory failure because it improves gas exchange and rests respiratory muscles. During controlled mechanical ventilation, a patient’s inspiratory muscles are resting and the ventilator delivers a preset tidal volume through the generation of inspiratory flow, overcoming resistive and elastic thresholds of the respiratory system. During assisted ventilation, the same goal is reached through an interplay between the patient’s inspiratory muscles and ventilator. Every perturbation of this interaction causes patient ventilator asynchrony and exposes to the risk of failure to ventilate. Patient–ventilator asynchrony may occur at each stage of assisted breath Signs of patient’s discomfort, the use of accessory muscles, tachycardia, hypertension, and assessment of flow and airway pressure traces displayed on modern ventilators, helps to detect asynchronies. Prompt recognition and intervention to improve patient–ventilator interaction may expedite liberation from mechanical ventilation, and reduce intensive care unit and length of hospital stay.

Positive-end-expiratory pressure (PEEP) is the pressure present in the airway (alveolar pressure) above atmospheric pressure that exists at the end of expiration. The term PEEP is defined in two particular settings. Extrinsic PEEP (applied by ventilator) and intrinsic PEEP (PEEP caused by non-complete exhalation causing progressive air trapping). Applied (extrinsic) PEEP—is usually one of the first ventilator settings chosen when mechanical ventilation (MV) is initiated. Applying PEEP increases alveolar pressure and volume. The increased lung volume increases the surface area by reopening and stabilizing collapsed or unstable alveoli. PEEP therapy can be effective when used in patients with a diffuse lung disease with a decrease in functional residual capacity. Lung protection ventilation is an established strategy of management to reduce and avoid ventilator-induced lung injury and mortality. Levels of PEEP have been traditionally used from 5 to 12 cmH2O; however, higher levels of PEEP have also been proposed and updated in order to keep alveoli open, without the cyclical opening and closing of lung units (atelectrauma). The ideal level of PEEP is that which prevents derecruitment of the majority of alveoli, while causing minimal overdistension; however, it should be individualized and higher PEEP might be used in the more severe end of the spectrum of patients with improved survival. A survival benefit for higher levels of PEEP has not been yet reported for any patient under MV, but a higher PaO2/FiO2 ratio seems to be better in the higher PEEP group.

Respiratory adverse events are the commonest complications after anaesthesia and have profound implications for the recovery of the patient and their subsequent health. Outcome prediction related to respiratory disease and complications is vital when determining the risk:benefit balance of surgery and providing informed consent. Surgery produces an inflammatory response and pain, which affects the respiratory system. Anaesthesia produces atelectasis, decreases the drive to breathe, and causes muscle weakness. As the respiratory system ages, closing capacity increases and airway closure becomes an increasing issue, resulting in atelectasis. Increasing comorbidity and polypharmacy reduces the patient’s ability to eliminate drugs. The proportion of major operations on older frailer patients is rising and postoperative recovery becomes more complicated and the demand for critical care rises. At the same time, the population is becoming more obese, producing rapid decreases in end-expiratory lung volume on induction, together with a high incidence of sleep-disordered breathing. Despite this, many high-risk patients are not accurately identified preoperatively, and of those that are admitted to critical care, some are discharged and then readmitted to the intensive care unit with complications. Respiratory diseases may lead to increases in pulmonary vascular resistance and increased load on the right heart. Some lung diseases are primarily fibrotic or obstructive. Some are inflammatory, autoimmune, or vasculitic. Other diseases relate to the drive to breathe, the nerve supply to, or the respiratory muscles themselves. The range of types of respiratory disease is wide and the physiological consequences of respiratory support are complex. Research continues into the best modes of respiratory support in theatre and in the postoperative period and how best to protect the normal lung. It is therefore essential to understand the effects of surgery and anaesthesia and how this impacts existing respiratory disease, and the way this affects the balance between load on the respiratory system and its capacity to cope.

Disorders affecting the lower cranial nerves – V (trigeminal), VII (facial), IX (glossopharyngeal), X (vagus), XI (accessory) and XII (hypoglossal) – are discussed in the first part of this chapter. The clinical neuroanatomy of each nerve is described in detail, as are disorders – often in the form of lesions – for each nerve.Trigeminal nerve function may be affected by supranuclear, nuclear, or peripheral lesions. Because of the wide anatomical distribution of the components of the trigeminal nerve, complete interruption of both the motor and sensory parts is rarely observed in practice. However, partial involvement of the trigeminal nerve, particularly the sensory component, is relatively common, the main symptoms being numbness and pain. Reactivation of herpes zoster in the trigeminal nerve (shingles) can cause pain and a rash. Trigeminal neuralgia and sensory neuropathy are also discussed.Other disorders of the lower cranial nerves include Bell’s palsy, hemifacial spasm and glossopharyngeal neuralgia. Cavernous sinus, Tolosa–Hunt syndrome, jugular foramen syndrome and polyneuritis cranialis are caused by the involvement of more than one lower cranial nerve.Difficulty in swallowing, or dysphagia, is a common neurological problem and the most important consequences include aspiration and malnutrition (Wiles 1991). The process of swallowing is a complex neuromuscular activity, which allows the safe transport of material from the mouth to the stomach for digestion, without compromising the airway. It involves the synergistic action of at least 32 pairs of muscles and depends on the integrity of sensory and motor pathways of several cranial nerves; V, VII, IX, X, and XII. In neurological practice dysphagia is most often seen in association with other, obvious, neurological problems. Apart from in oculopharyngeal muscular dystrophy, it is relatively rare as a sole presenting symptom although occasionally this is seen in motor neurone disease, myasthenia gravis, and inclusion body myositis. Conversely, in general medical practice, there are many mechanical or structural disorders which may have dysphagia as the presenting feature. In some of the disorders, notably motor neurone disease, both upper and lower motor neurone dysfunction may contribute to the dysphagia. Once dysphagia has been identified as a real or potential problem, the patient should undergo expert evaluation by a clinician and a speech therapist, prior to any attempt at feeding. Videofluoroscopy may be required. If there is any doubt it is best to achieve adequate nutrition through the use of a fine-bore nasogastric tube and to periodically reassess swallowing. Anticholinergic drugs may be helpful to reduce problems with excess saliva and drooling that occur in patients with neurological dysphagia, and a portable suction apparatus may be helpful. Difficulty in clearing secretions from the throat may be helped by the administration of a mucolytic agent such as carbocisteine or provision of a cough assist device.

Any public debate about air pollution starts with the premise that air pollution cannot be good for you, so we should have less of it. However, it is much more difficult to determine how much is dangerous, and even more difficult to decide how much we are willing to pay for improvements in measured air pollution. Recent UK estimates suggest that fine particulate pollution causes about 6500 deaths per year, although it is not clear how many years of life are lost as a result. Some deaths may just be brought forward by a few days or weeks, while others may be truly premature. Globally, household pollution from cooking fuels may cause up to two million premature deaths per year in the developing world. The hazards of black smoke air pollution have been known since antiquity. The first descriptions of deaths caused by air pollution are those recorded after the eruption of Vesuvius in ad 79. In modern times, the infamous smogs of the early twentieth century in Belgium and London were clearly shown to trigger deaths in people with chronic bronchitis and heart disease. In mechanistic terms, black smoke and sulphur dioxide generated from industrial processes and domestic coal burning cause airway inflammation, exacerbation of chronic bronchitis, and consequent heart failure. Epidemiological analysis has confirmed that the deaths included both those who were likely to have died soon anyway and those who might well have survived for months or years if the pollution event had not occurred. Clean air legislation has dramatically reduced the levels of these traditional pollutants in the West, although these pollutants are still important in China, and smoke from solid cooking fuel continues to take a heavy toll amongst women in less developed parts of the world. New forms of air pollution have emerged, principally due to the increase in motor vehicle traffic since the 1950s. The combination of fine particulates and ground-level ozone causes ‘summer smogs’ which intensify over cities during summer periods of high barometric pressure. In Los Angeles and Mexico City, ozone concentrations commonly reach levels which are associated with adverse respiratory effects in normal and asthmatic subjects. Ozone directly affects the airways, causing reduced inspiratory capacity. This effect is more marked in patients with asthma and is clinically important, since epidemiological studies have found linear associations between ozone concentrations and admission rates for asthma and related respiratory diseases. Ozone induces an acute neutrophilic inflammatory response in both human and animal airways, together with release of chemokines (e.g. interleukin 8 and growth-related oncogene-alpha). Nitrogen oxides have less direct effect on human airways, but they increase the response to allergen challenge in patients with atopic asthma. Nitrogen oxide exposure also increases the risk of becoming ill after exposure to influenza. Alveolar macrophages are less able to inactivate influenza viruses and this leads to an increased probability of infection after experimental exposure to influenza. In the last two decades, major concerns have been raised about the effects of fine particulates. An association between fine particulate levels and cardiovascular and respiratory mortality and morbidity was first reported in 1993 and has since been confirmed in several other countries. Globally, about 90% of airborne particles are formed naturally, from sea spray, dust storms, volcanoes, and burning grass and forests. Human activity accounts for about 10% of aerosols (in terms of mass). This comes from transport, power stations, and various industrial processes. Diesel exhaust is the principal source of fine particulate pollution in Europe, while sea spray is the principal source in California, and agricultural activity is a major contributor in inland areas of the US. Dust storms are important sources in the Sahara, the Middle East, and parts of China. The mechanism of adverse health effects remains unclear but, unlike the case for ozone and nitrogen oxides, there is no safe threshold for the health effects of particulates. Since the 1990s, tax measures aimed at reducing greenhouse gas emissions have led to a rapid rise in the proportion of new cars with diesel engines. In the UK, this rose from 4% in 1990 to one-third of new cars in 2004 while, in France, over half of new vehicles have diesel engines. Diesel exhaust particles may increase the risk of sensitization to airborne allergens and cause airways inflammation both in vitro and in vivo. Extensive epidemiological work has confirmed that there is an association between increased exposure to environmental fine particulates and death from cardiovascular causes. Various mechanisms have been proposed: cardiac rhythm disturbance seems the most likely at present. It has also been proposed that high numbers of ultrafine particles may cause alveolar inflammation which then exacerbates preexisting cardiac and pulmonary disease. In support of this hypothesis, the metal content of ultrafine particles induces oxidative stress when alveolar macrophages are exposed to particles in vitro. While this is a plausible mechanism, in epidemiological studies it is difficult to separate the effects of ultrafine particles from those of other traffic-related pollutants.