Over the past several decades, a spectrum of adverse health effects have been attributed to poor indoor air quality encountered in indoor ice arenas. Numerous contaminants and toxicants have been detected, the most important of which, carbon monoxide (CO) and nitrogen dioxide (NO₂), are produced during ice resurfacing. Other compounds produced during ice resurfacing, including other oxides of nitrogen, aldehydes, volatile organic compounds and respirable-range particulate matter, may also contribute to disease. The total burden of illness and impairment (transient or chronic) attributable to poor indoor air quality in arenas is unknown, but may be quite significant. One analysis carried out in the late 1990s of 332 rinks in nine countries reported excess concentrations of NO₂ in 40% of the rinks.

Ice arenas are found throughout many communities worldwide, especially across Europe and North America. Multiple sports utilize indoor ice arenas, including ice hockey, figure skating, recreational ice skating, short track speed skating and curling. Ice hockey is among the world’s most popular sports with tens of millions of participants in youth and adult leagues worldwide. Since air quality monitoring in ice arenas varies across venues, if present at all, details about the scope of the problem and the public health impact of poor indoor air quality in indoor ice arenas cannot be precisely established. Moreover, since exposures to indoor ice arena air pollutants such as CO and NO₂ typically produce nonspecific signs and symptoms and, because many of their health effects are typically short-lived and self-limited after the exposure abates, it is likely that a significant burden of disease attributable to poor ice arena air quality is not recognized.

Poor indoor air quality in ice arenas may result from a variety of environmental and engineering factors including ventilation system deficiencies, tobacco smoke, faulty heating systems, cleaning chemicals, refrigerants and mold contamination. A discussion of all possible point sources for poor indoor air quality is beyond the purview of this chapter. The principle focus of this section is ice resurfacing equipment exhaust, a major point source for pollutants in most arenas, and the health effects attributable to this exposure.

Most ice resurfacers, including ‘Zamboni machines’, utilize combustion engines that operate with a fossil fuel (e.g. gasoline and propane) and produce exhaust with a mixture of hazardous compounds, including CO and oxides of nitrogen, especially NO₂, as well as volatile organic compounds and respirable-range particulate matter. While there is nothing remarkable about the exhaust produced from ice resurfacing equipment, the machines present a special hazard in indoor ice arenas because they operate repeatedly, starting and stopping, in what is essentially a confined space. Just as running a motor vehicle inside of a closed garage can produce a hazardous exposure setting, the operation of ice resurfacing equipment inside a poorly ventilated arena can result in significant indoor air pollution.

The concentration of compounds present in the exhaust of ice resurfacing equipment is partially a function of the temperature of the engine. CO production is greatest when an engine has been newly started and is running at a relatively low temperature. As the machine warms, CO production decreases while the production of oxides of nitrogen, including NO₂, increases. Accordingly, concentrations of exhaust pollutants from ice resurfacing equipment inside an arena will, in part, depend upon on the frequency of equipment start-stop cycles and the duration that the engine runs during each cycle, as well as venue characteristics such as size and air exchange rate.

The clinical syndromes attributable to ice arena air pollution are generally abrupt in onset and unfold over a relatively short time frame: minutes to hours. Health effects resulting from long-term exposure to low-level concentrations of airborne pollutants encountered in indoor ice arenas are not well established. While the relationships between chronic exposure to exhaust pollutants and cardiopulmonary and neurocognitive outcomes are of epidemiologic interest, it unlikely that a causal link between low-level indoor ice arena air pollution and a chronic health effect can be established with confidence at the level of the single individual.

Operators of ice resurfacing equipment are at obvious risk of exposure to equipment exhaust as a consequence of their proximity to the point source and their repeated exposure to exhaust throughout their work shift. Athletes and sports participants are also at special risk because of the duration of exposure (i.e. time spent on the ice) and especially because of their increased ventilation and metabolic demands resulting from vigorous aerobic exercise.

Confirmation of exposure to CO can be established through testing of peripheral blood specimens for carboxyhemoglobin in a clinical laboratory. In contrast, detection of exposure to most other toxic gases, including NO₂, requires air sampling in the field by an industrial hygienist.

Diagnosis of an adverse health effect attributable to airborne pollutants in an indoor ice arena begins with the history. First, the clinician must suspect that an illness or symptom may be attributable to a toxic environmental exposure. Second, the clinician must act on the suspicion and gain data that supports or refutes the hypothesis. As is the case with other exposure settings and environmental illnesses, the patient may be the first person to consider a possible relationship between either a specific toxicant or exposure setting and the illness. In such instances, the process of establishing a diagnosis will be facilitated by the patient’s presenting complaint (e.g. ‘I am always the first person on the ice after the Zamboni machine finishes resurfacing because I like to take advantage of the excellent skating conditions, but I have noticed, lately, I develop headaches and dizziness when I start skating which tend to get better on their own.’). Patient recognition of causation commonly occurs when there is an extreme exposure with a manifestly clear cause and effect relationship (e.g. a major mishap, accident or evident equipment malfunction), or a cluster of cases (e.g. multiple affected teammates) that point to etiology. In cases where causation is not obvious, the clinician will need to make the link between the exposure setting and possible etiologic toxicants and the disorder.

Workers, athletes and spectators may be exposed to ice arena toxicants. Accordingly, the occupational history may elucidate causation for some affected individuals (i.e. employees who work in ice arenas, such as drivers of ice resurfacing machines) and, in turn, facilitate diagnosis of the illness. However, in others, an environmental history that considers hobbies, pastimes and athletic activities (i.e. participation in an ice sport) will be necessary to identify the exposure-disorder relationship.

The major disorders attributable to ice arena air pollution are CO intoxication and NO₂ pneumonitis. Strictly defined, carbon monoxide intoxication is not a disorder of the lungs. While the respiratory tract is the portal of entry for carbon monoxide, adverse health effects caused by carbon monoxide largely cause dysfunction of other organ systems. In contrast, the respiratory tract is both the route of exposure and the target organ in NO₂ related illness.

Carbon monoxide is the gas most often reported as a cause of intoxication in indoor ice arenas. CO is a nonirritating, tasteless, odorless and colorless gas formed by hydrocarbon combustion and an important component of the exhaust of ice resurfacing equipment. CO diffuses readily across the alveolar-capillary interface and binds with avidity to hemoglobin, forming carboxyhemoglobin (COHb), which results in compromised oxygen transport and utilization. In addition to competing with oxygen for the heme moiety of hemoglobin, CO also compromises the ability of the other heme moieties with bound oxygen to offload oxygen to peripheral tissues. CO also interferes with peripheral oxygen utilization. These CO effects are independent of those on hemoglobin and oxygen delivery.

The uptake of CO increases with exercise. Studies of CO concentrations in hockey players have found a linear relationship between COHb levels and exposure time and concentrations of ambient CO. Investigators found a 1.0% rise in COHb for each 10 parts per million (ppm) of ambient CO in an indoor arena during a 90 minute hockey game. Other investigators found a CO concentration of approximately 22 ppm raised COHb levels in hockey players to greater than 3% from a baseline of 1%, on average. Concentrations of CO exceeding 20 ppm in indoor ice arenas have been described in numerous reports. The United States Environmental Protection Agency National Ambient Air Quality Standard for CO is 9 ppm time weighted average over 8 h.

The clinical findings of CO poisoning are nonspecific and vary based on severity of intoxication. COHb levels less than 2.5% are typically inconsequential. COHb concentrations between 2.5 and 10% may affect vision, manual dexterity and exercise tolerance. Concentrations greater than 20% can cause headaches, dizziness, malaise and nausea. Severe CO intoxication may result in seizures, coma and myocardial ischemia, and dysrhythmias. Severe intoxication in an indoor ice arena would only result from an unusual mishap such as the running (e.g. idling) of an ice resurfacing engine inside of a small confined space within the larger enclosed ice arena.

Acute CO poisoning is first suspected on the basis of a suggestive history. Confirmation of intoxication requires a COHb level measured by co-oximetry of a blood gas sample. Moderate- to high-intensity exposures, especially in patients with underlying coronary artery disease, warrant further evaluation to assess for myocardial ischemia, including an electrocardiogram and measurement of cardiac enzymes. The most important interventions in the management of CO intoxication are removal of the affected individual from the CO source and institution of high-flow oxygen by face mask. The role of hyperbaric oxygen therapy remains controversial and is unlikely to be required to manage the low-level intoxication typically encountered in indoor ice arenas. Indeed, because symptoms of exposure (e.g. headaches and diminished exercise capacity) may be interpreted as a nuisance by the affected individual rather than a major health problem, an important consideration is the possibility of repeated low-level intoxication that goes undetected. Moreover, an affected individual (e.g. enthusiastic athlete) may not be receptive to counseling to avoid the potentially toxic environment. Suspicion of ice arena intoxication should prompt assessments of engineering controls at the venue.

Nitrogen dioxide is another gas that may be encountered in hazardous concentrations in indoor ice arenas, although disorders attributable to NO₂ exposure have not been reported as commonly as CO intoxication. NO₂ is a reddish-brown gas with a characteristic sharp, biting odor. The principle point source for NO₂ is the internal combustion engine of an ice resurfacing machine. NO₂ is heavier than most of the constituent gases in air and tends to remain close to the surface of the ice. NO₂ causes respiratory tract injury that may range from mild irritation with minimal short-term clinical consequences to acute lung injury with significant symptoms and respiratory impairment. Chest tightness, wheezing, asthma flares and cough may be caused by NO₂ inhalation. NO₂ is relatively water-insoluble and therefore does not typically produce classic symptoms of irritation upon initial exposure. The lack of ‘warning symptoms’ can result in significant exposure over hours before any symptoms of injury develop. NO₂ is a powerful oxidant and also slowly combines with water in the respiratory tract to produce nitric and nitrous acid which may contribute to lung injury.

In one of the best described exposure incidents, an outbreak of NO₂-induced respiratory illness occurred among players and spectators at two high school hockey games played at an indoor ice arena in Minnesota, USA. The source of the NO₂ was the malfunctioning engine of the ice resurfacer. Affected individuals experienced acute onset of cough, hemoptysis and/or dyspnea during attendance or within 48 hours of attending a hockey game. In all, 116 cases were identified among hockey players, cheerleaders and band members who attended the two games. Members of two hockey teams had spirometry performed at 10 days and 2 months after exposure; no significant compromise in lung function was documented.

Swedish investigators reported two cases of toxic pneumonitis with delayed onset in hockey players due to NO₂ exposure during an ice hockey game in an indoor arena. Signs and symptoms included cough, hemoptysis, dyspnea and reduced peak expiratory flow. The chest radiographs showed reticulo-nodular opacities in one player and patchy consolidation in the second player. Repeat chest radiographs obtained within one week of exposure were normal in both cases.

It is unknown to what extent athletic performance may be adversely affected by ‘subclinical’ exposures to NO₂ in indoor ice arenas.

There is no specific therapy for NO₂ pneumonitis. Bronchodilators are appropriate to treat airflow obstruction and inhaled corticosteroids may reduce airway inflammation. The role of systemic corticosteroids is not established, but should be considered with high-intensity exposures.

Mixed exhaust exposures have also been linked with respiratory illness. Chronic cough and dyspnea were reported in ice hockey players after an acute exposure to a faulty ice resurfacer. In one report of 16 previously healthy hockey players, more than half complained of cough and dyspnea on exertion 6 months post-exposure. All had normal pulmonary function tests, exercise studies and chest computed tomographs. Additional testing using impulse oscillometry showed evidence of increased airway resistance and small airway disease.

Standards addressing air quality in indoor ice arenas have been developed and published. A Canadian agency has recommended average concentrations for CO and NO₂ to be lower than those in work environments. The United States National Ambient Air Quality Standard for carbon monoxide is 9 ppm time-weighted average over 8 hours and 35 ppm over 1 hour, and for NO₂ 0.053 ppm (53 parts per billion, ppb) annual average. Additional Canadian guidelines for the operation of ice resurfacers with internal combustion engines include: (1) regular testing of ice resurfacer equipment emissions; (2) installation of monitors to measure the concentration of toxic gases at the opening of the exhaust pipe; (3) use of a catalytic purifier; (4) operation of resurfacers by an experienced operator to minimize time of equipment operation; (5) 90 minute intervals between resurfacing; (6) open rink doors during and after resurfacing; (6) air quality standards of 1 hour maximal allowable exposure to CO at 20 ppm and NO₂ at 200 ppb; (7) regular monitoring of ambient air in indoor ice rinks; (7) installation of warning signs that describe the potential symptoms and hazards of CO and NO₂ poisoning; (8) educational seminars for rink staff, coaches, parents and patrons of ice rinks; and (9) development of an emergency plan in the case of an intoxication incident.

A potentially transformative engineering control has been the development of the electric ice resurfacing machine which does not emit exhaust fumes. As they are more costly than internal combustion models, replacement of internal combustion models with electric-powered ones may not be possible in many ice arenas, but if carried out would result in improved indoor air quality.

Cold air can produce bronchoconstriction and provoke asthma exacerbations. Indeed, cold air challenges are used in some clinical pulmonary function laboratories to test for the presence of bronchial hyperresponsiveness, a hallmark of asthma. The combination of exposure to cold air and intense exercise contributes to dyspnea and provokes asthma in a significant minority of endurance athletes. The prevalence of asthma in elite athletes has been reported to be as high as 20%. Some individuals intolerant of intense exercise in cold air may avoid cold weather sports, resulting in a ‘healthy athlete effect’ and an underestimation of the total population affected by the co-exposures. Diagnosis of bronchoconstriction provoked by exercise in cold air may be facilitated by serial peak expiratory flow monitoring before, during and following exposure. The use of inhaled beta agonists before participation in cold weather sports is advisable for individuals with evidence of exercise-induced bronchoconstriction, and should be considered for athletes who experience dyspnea out of proportion to their exertion, or dyspnea that does not resolve with cessation of exercise. A trial of beta-2 agonist therapy may help to confirm the diagnosis of asthma, as well as offer relief to the sports participant.

Importantly, not all dyspnea associated with exercise in cold air is due to broncho-constriction. Reflex mechanisms in some individuals that reduce minute ventilation in response to cold air inhalation may contribute to dyspnea. Bronchodilators are not likely to be beneficial in these settings because bronchoconstriction is not a hallmark of the condition.

Swimming is a widely popular sport among people of all ages. In 2005 it was estimated that the number of Americans swimming for fitness was about 16 million. Learning how to swim is mandatory at the elementary school level in the UK and swimming is among the most popular forms of exercise among adults. Other competitive and recreational indoor water sports include water polo, springboard diving and synchronized swimming. Spas and fitness centers with hot water tubs, jet pools and saunas are additional indoor settings where the hazards of indoor water sports may be encountered.

While the respiratory disorders associated with water sports are seen in both the indoor and outdoor setting, the indoor setting presents special risks. This is attributable to multiple factors including reduced ventilation, differences in pool maintenance requirements and micro-climates around indoor swimming arenas with higher temperature and humidity. The population at highest risk includes those who use such facilities with regularity, or workers such as lifeguards, trainers and cleaning and maintenance staff.

The more common pulmonary disorders attributable to indoor water sports include: (1) asthma – exacerbations of pre-existing asthma and irritant-induced asthma; (2) extrinsic allergic alveolitis – also known as hypersensitivity pneumonitis; (3) nontuberculous mycobacterial infection (especially Mycobacterium avium and Mycobacterium intracellulare); (4) swimming-induced pulmonary edema; and (5) pulmonary contusion and pneumothorax.

In an unscientific survey of 220 participants at the interactive occupational grand round of the 1998 annual European Respiratory Society meeting in Geneva, about half the audience had either definitely or probably seen cases of swimming pool asthma. Most of these participants spent <10% of their practice time treating occupational lung disorders. Swimming pool cleaning staff are at special risk of respiratory tract injury and disease resulting from mishaps involving disinfectants, including mixing incompatibilities (e.g. bleach with ammonia or acids).

A Dutch study collected samples from 38 swimming pool facilities and questionnaires from 624 workers at these facilities. They found a higher incidence of pulmonary atopy-related complaints among the workers compared with the general population. High levels of chloramine exposure correlated with greater frequency of pulmonary complaints. However, there are conflicting data that have resulted in children with asthma being encouraged to take up swimming because of the perceived benefit of breathing moist air.

Elite swimmers have a higher incidence of bronchial hyperresponsiveness compared with the general population. Certain investigators have hypothesized that swimming in chlorinated pools potentiates lung damage and may be partly responsible for the increasing incidence of asthma in Western societies. This conclusion is based on the observation of elevated levels of serum pneumoproteins in children who frequently attend chlorinated swimming pools compared with controls. The elevated levels of serum pneumoproteins are believed to reflect increased alveolar-capillary permeability and early lung injury.

The United States Centers for Disease Control and Prevention recently reported an analysis of a large number of guests at two separate hotels who were exposed to high levels of chloramine-like compounds near the indoor swimming pool area and experienced significant ocular and respiratory symptoms. Events such as these underscore the importance of staff training, proper ventilation and appropriate handling of compounds used for disinfection. Public health departments are encouraged to adhere to guidelines for cleaning and maintenance of swimming pools, to ensure ventilation and minimize exposure to volatile compounds, and to educate the public about proper pool hygiene.

Exposure to certain chlorine-derived compounds or ozone can cause or exacerbate asthma. Asthma symptoms including cough, wheezing, chest tightness, dyspnea at rest or with exercise and reduced exercise capacity are usually temporally linked to either routine use of the pool or to exposures to high concentrations of chemicals (either unregulated or during shock treatment). Patients often feel better during days when they are not in the pool environment. The physical and laboratory findings in these patients may include wheezing, a prolonged expiratory phase, hypocapnea and hypoxemia on arterial blood gas measurement, especially during an exacerbation. Serial assessments of peak expiratory flow rate and pulmonary function testing are commonly part of the evaluation. Radiographs are often unremarkable, though hyperinflation may be seen in severe cases. If patients are symptomatic, but have nondiagnostic pulmonary function test results, bronchoprovocation testing with methacholine (methacholine challenge test) can provide important diagnostic information.

Management consists of avoiding the pool and the surrounding environment if the symptoms are severe and debilitating. If it appears that a large number of users are developing similar symptoms, then the pool maintenance staff must test the water quality, ensure proper treatment of pools by using recommended practices, and also test air quality around the pool area with the objective that proper ventilation is maintained. Pharmacologic treatment is no different than that for other cases of asthma and includes corticosteroids and bronchodilators. Systemic corticosteroids may be used for severe exacerbations.

The indoor pool environment presents the risk of an accidental high intensity exposure to water treatment chemicals. Such an exposure may cause severe respiratory tract irritation resulting in acute irritant-induced asthma. The hallmark features of irritantinduced asthma include a high-intensity exposure resulting in the abrupt onset of symptoms of increased airway reactivity, often within minutes of exposure. An important clinical reminder for physicians is that some patients manifest worsening symptoms after initial improvement or after a latency period of 6-12 hours after exposure. Therefore it is important to monitor individuals involved in major chemical spills and mishaps in a controlled setting for at least 24 hours. Acute irritant-induced asthma may improve over time or persist. It is necessary to prevent recurrent high intensity exposure to the offending agent. However, low-level exposure to the irritant agent is typically tolerated, so exposed individuals can typically return to the pool environment. Pharmacological management is similar to that for other presentations of asthma.

Extrinsic allergic alveolitis (EAA), also known as hypersensitivity pneumonitis, is an immunologic non-IgE mediated inflammatory lung disease that results from prior sensitization and subsequent exposure to specific organic and inorganic antigens in the atmosphere. It has been studied and investigated in both outdoor and indoor swimming pools, hot water tubs, spas and saunas. Factors associated with EAA include: