Chapter 7: Respiratory Toxicants of Interest to Pet Owners

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Respiratory Toxicants of Interest to Pet Owners



Poor air quality, either indoor (i.e., residential) or outdoor (i.e., ambient), can cause or contribute to development of disease in humans and pets. Consequently, owners may approach their veterinarian with questions about the potential for airborne toxins to negatively impact the health of their pets. Such toxicants include biologic materials (e.g., allergens, microbes, and mycotoxins), gaseous pollutants, volatile organic chemicals (VOCs), particles, dust, and fibers. These agents are associated with increased risk of developing respiratory and neurologic signs, chronic respiratory inflammation, allergies, and neoplasia. The cause of these disorders can be difficult to establish because of the nonspecificity of clinical signs and because multiple etiologies may be involved. Because most birds, cats, and dogs spend the majority of their lives within the family residence, this chapter focuses on commonly encountered indoor toxicants and related home conditions. Ambient air pollutants that readily permeate indoor spaces also are included. Approaches for improving indoor air quality (IAQ) are discussed in brief.


Disclaimer: This information has been reviewed by the National Health and Environmental Effects Research Laboratory, U.S. EPA, and approved for publication. Approval does not signify that the contents necessarily reflect the views and policies of the agency, nor does the mention of commercial products constitute endorsement.



Biologic Contaminants



Allergens


Data linking respiratory disease in companion animals to allergen exposure are limited in part by lack of commercially available, validated, allergen-specific antibody assays for pets. Supportive evidence comes from beneficial clinical responses to allergen avoidance, as well as from studies demonstrating that cats with bronchial disease have significantly more positive intradermal skin test reactions to dust mite (a common indoor aeroallergen) than do healthy cats (Moriello et al, 2007). Similarly, allergen-specific immunoglobulin E (IgE) testing in serum of affected cats showed strong reactivity to dust mite and regional outdoor aeroallergens (Norris Reinero et al, 2004). In humans, there is increasing evidence that IgE antibodies to dust mites, cockroaches, and pets are causally related to lung inflammation and asthma. Although pet exposure can undoubtedly worsen allergy symptoms in sensitized individuals, low levels of dog (Can f 1) or cat (Fel d I) allergens are universally present in U.S. homes—even in those without pets for long periods. Moreover, there are data to suggest that pet exposure during childhood may help to avert development of allergic sensitization. This protective pet effect is influenced by host factors (genetics, sex); the type of pet (dog, cat, or both); and the level, timing/duration, and route of allergen exposure (e.g., inhaled versus oral ingestion of allergens in dust). Through stimulation of the innate immune system early in life (especially year one), proallergic immune responses are in some manner modified, thus facilitating long-lasting species-specific immunologic tolerance (Platts-Mills, 2011; Bernstein, 2012).



Dampness and Mold


As residential energy costs rose over the past 40 years, houses became more efficiently insulated and airtight. By increasing mechanical recirculation of indoor air, the volume of outdoor air entering a dwelling could be reduced, thus making homes more economical to heat and cool. Unfortunately, such changes also lead to more stagnant and humid indoor air—effects that in combination with extensive wall-to-wall carpeting allow microorganisms and house dust (including mites and their excreta) to accumulate at concentrations higher than previously encountered. Tight building syndrome is especially problematic if residential heating, ventilation, and air conditioning (HVAC) systems are not functioning optimally and when water intrusion into the home occurs (from floods, hurricanes, or plumbing, appliance, and roof leaks). Excessive moisture leads to growth of mold, other types of fungi, and bacteria, which subsequently emit spores, hyphae fragments, microbial VOCs, and endotoxin into the indoor air (Cabral, 2010).


The U.S. Institute of Medicine (2004) concluded that there is sufficient evidence of an association between dampness and adverse health outcomes; however, causality has not yet been established. Home dampness may serve as a marker for generalized increases in dust and other products that accumulate during conditions of reduced ventilation. Alternatively, dampness may be a proxy for mold and its secreted metabolites, which include enzymes, hemolysins, β-D-glucans, and potent mycotoxins (e.g., macrocyclic trichothecenes, aflatoxins, satratoxins, gliotoxins, and chaetoglobosins).


Linking specific biocontaminants to particular respiratory or neurologic syndromes remains an area of active investigation and debate. Microbial VOCs, for example, are known ocular and upper respiratory tract irritants. Furthermore, biocontaminants can cause respiratory and systemic infection, as epitomized by Legionnaire’s disease, (which can arise from overgrowth of the bacterium Legionella within air conditioning systems). Biocontaminants are also implicated in hypersensitivity responses (e.g., pneumonitis, chronic rhinosinusitis), exacerbation of allergies and asthma, and chronic neurologic conditions (Thrasher and Crawley, 2009). Cats, not unlike young children, may be exposed to these agents both through inhalation and via ingestion of house dust (cats due to extensive grooming and kids due to increased floor contact time and “mouthing” behaviors). A recent report describing acute pulmonary hemorrhage and death of two cats exposed to toxic black mold was remarkably similar to a cluster of cases in infants in the Cleveland area who also developed pulmonary hemorrhage. Indicative of Stachybotrys chartarum exposure, satratoxin G adducts were detected in archived serum samples from the cats. Concurrent stressors of cigarette smoke and inhalant anesthesia may have contributed to the lung changes observed (Mader et al, 2007). Novel approaches to define and quantify (1) indoor biocontaminant mass (e.g., quantitation of hydrophilic fungi or ergosterol in dust) (Park et al, 2008) and (2) exposure metrics (e.g., detection of mycotoxins in urine) (Straus, 2011) are critical to improving understanding of the spectrum of health effects associated with damp indoor environments.



Chemical Toxicants



Combustion-Derived Products


Second-hand smoke (SHS) is simply the smoke from someone else’s cigarette. It contains both gases and respirable particles that, particularly in poorly ventilated air spaces, can cause ocular and respiratory tract irritation. This is especially problematic for young children, in whom exposure is associated with wheeze, asthma exacerbation, and reduced resistance to infections, leading to increased incidence of otitis media, bronchiolitis, and pneumonia. The Surgeon General has concluded that there is no risk-free level of exposure to SHS, and thus a smoke-free environment is the only way to fully protect nonsmokers from the hazards of SHS (U.S. Department of HHS, 2010). Based on urinary levels of cotinine, a nicotine metabolite, house pets are similarly exposed to SHS, with levels in dogs increasing proportionately with the number of cigarettes smoked in the household (Bertone-Johnson et al, 2008). Therefore predisposition toward analogous conditions in exposed pets is likely, and by extension pets with preexisting upper or lower respiratory disease may be especially sensitive to the irritating effects of SHS. SHS exposure has also been associated with decreased pulmonary function (e.g., functional reserve capacity) in a pilot study of healthy dogs (Abrams et al, 2007) but was not identified as a significant risk factor for canine chronic cough (Hawkins et al, 2010).


Because sidestream cigarette smoke is generated at lower temperatures and under different conditions than mainstream (exhaled) smoke, SHS contains higher concentrations of certain carcinogens (e.g., polycyclic aromatic hydrocarbons [PAHs]). Hence SHS has been dually designated as a known human carcinogen and an occupational carcinogen. SHS exposure during childhood and adolescence can increase the risk of developing lung cancer as much as or more than exposure in adulthood (Asomaning et al, 2008). Limited studies associating SHS exposure with cancer in pets exist. In one study, increased risk for lung cancer was restricted to brachycephalic and mesocephalic dog breeds. Conversely, other reports showed dolichocephalic breeds were at increased risk for nasal cancer (Reif et al, 1998). Breed sensitivities notwithstanding, it is postulated that these associations reflect efficient trapping of carcinogens in the nasal cavity of dolichocephalic breeds, thereby minimizing lower airway deposition. Unfortunately, increased nasal retention may lead to increased risk of nasal cancer. In cats, SHS exposure is associated with risk for malignant lymphoma (Bertone et al, 2002) and oral squamous cell carcinoma (Snyder et al, 2004), likely reflecting both inhalation and oral (via grooming) routes of exposure. Relatedly, ingestion of cigarette butts is not uncommon in pets. Due to nicotine toxicity, this may prove fatal in birds and small dogs.



Air Pollutants


While catastrophic air pollution episodes were infamous for their toll on human life as in the London Fog of 1952, they also caused morbidity and mortality in animals. Precipitated by industrial accidents and temperature inversion patterns, North American disasters included Donora, PA (1948), when effluents from steel, zinc, and sulfuric acid plants became trapped in a valley inversion and 20 people, 10 dogs, 3 cats, and 40% of poultry in four nearby flocks died after developing respiratory signs, and Poza Rica, Mexico (1950), when hydrogen sulfide released into the ambient air during a thermal inversion led to the death of 22 people and an undetermined number of dogs, swine, and cattle, as well as nearly 100% of the canaries in the area (Catcott, 1961).


Owing to pollution control regulations, present-day levels are greatly reduced but are still associated with significant economic toll due to health care costs and lost productivity. Health effects of individual air pollutants are summarized in the following section (based on epidemiologic associations and data from relatively short-term, high-dose experimental exposures). By contrast, real world exposures are chronic, are lower level, and involve multiple pollutants, which —owing to additive or synergistic effects—may culminate in significant health risk for children, the elderly, and people with cardiorespiratory disease. A recent pilot study of urban cats noted increasing prevalence of feline asthma over the last 20 years (Ranivand and Otto, 2008). Likewise, retrospective studies in dogs noted that older urban dogs (> 7 years old) had greater radiographic evidence of thoracic disease than either young dogs or older rural dogs (Reif, 1970) and that urban dogs had increased risk for oral (tonsillar) cancer (Ragland and Gorham, 1967).


Nitrogen dioxide (NO2), a poisonous, corrosive, brownish gas, is both a major indoor and outdoor air pollutant. The primary indoor sources are poorly ventilated biomass-burning (coal or wood fireplaces and stoves) and gas (e.g., water heaters, clothes dryers, kitchen ranges) appliances. When indoor sources combine with permeation of traffic emissions, indoor levels can exceed (by as much as five times) ambient NO2 concentrations, well in excess of levels considered safe in outdoor air by the U.S. Environmental Protection Agency (EPA). Adverse health effects of NO2 include impairment of immune defense mechanisms. Data suggest that infants and children with atopy or asthma are more sensitive to the respiratory effects of NO2, in part due to enhanced asthmatic reactions to inhaled allergens (Bernstein et al, 2008). NO2 is also an atherogenic risk factor, especially in obese humans, and is associated with cardiovascular events and hospitalization. Long-term (near-lifetime) exposure to NO2 is also purported to contribute to chronic emphysematous lung changes. Thus in pets NO2 exposure may result in increased frequency and/or severity of respiratory infection and contribute to chronic bronchial and lung pathologic changes.


Carbon monoxide (CO) is a colorless, odorless gas. Unlike most air pollutants in which effects relate to low-level, chronic exposure, a single (likely to be encountered) exposure may prove lethal. Owing to its overt affinity for hemoglobin, CO prevents cellular oxidation, resulting in severe cellular anoxia. Initial clinical signs include vague lethargy, headache, and fatigue, progressing to confusion, nausea, and ultimately unconsciousness and death. As CO is a product of incomplete fuel combustion, its sources are similar to those of NO2, the primary one being motor vehicle exhaust. Classic cases of human poisonings, whether accidental or intentional, arise from car engines left running in attached garages or sheds. Significant exposure may also occur during use of charcoal grills or unvented kerosene heaters in relatively closed air spaces, or when chimneys or venting ducts of central heating systems are obstructed. Birds are especially sensitive to CO, as evidenced by their classic use as sentinels in coal mine shafts. CO poisoning is also an important cause of the morbidity and mortality in pets rescued from burning buildings. Having set clinic protocols in place for managing animal victims of smoke inhalation can help to ensure a successful outcome (Fitzgerald and Flood, 2006). For example, isocapnic hyperpnea with 100% O2 has been shown in dogs to double the rate of CO elimination compared with normal ventilation with 100% O2—a simple but effective means of hastening recovery of poisoned pets (Fisher et al, 1999). Cooperation with local firefighters to equip fire trucks with pet-sized face masks may allow for more effective O2 delivery on site, thus improving pet survival.


Ozone (O3), a potent oxidant gas, is among the most injurious of the ambient air pollutants. Exposure is associated with respiratory tract irritation, injury, and inflammation. Ozone is primarily an outdoor air pollutant that is produced in the lower atmosphere by photochemical reactions involving combustion products of gasoline (and other solvents) with oxygen and sunlight. Hot temperatures and stagnant air masses contribute to increased ambient concentrations. When significant accumulations occur near ground level, the phenomenon known as smog is observed. Indoor O3 levels arise mainly from outdoor levels permeating the home during normal air exchange. Indoor levels are usually less than half that of outdoor levels, but during smog episodes they may be sufficient to impact health. Ozone can also be emitted directly indoors by, for example, electric generators and office equipment such as photocopiers and laser printers. Ironically, ionizing air-purifiers intentionally generate O3 to react with and rid air of odors, resulting in indoor O3 concentrations that can exceed levels found in smog (Britigan et al, 2006).


In humans and laboratory animals, O3 has had variable effects on mucociliary clearance, a primary mechanism for clearing inhaled particles or offending microorganisms from the airways, thereby raising concerns about host resistance to infectious agents (Bernstein et al, 2008). In healthy dogs and humans, acute exposure can increase nonspecific airway responsiveness. In humans with atopic asthma, exposure to relatively low O3 concentrations (comparable to that of many urban areas) further augments the airway responsiveness increases noted during allergen challenge. Moreover, infant rhesus monkeys undergoing repeated exposure to O3, alternating with house dust mite allergen, developed significantly reduced lung capacity and long-lasting asthmalike disease (Schelegle et al, 2003). Data further suggest that O3 exposure can induce lipid oxidation and systemic vascular effects that—similar to NO2—may play a role in promoting atherosclerosis and associated cardiovascular disease.


Sulfur dioxide (SO2), another ambient air pollutant, is the major precursor to acidic deposition or so-called acid rain. Veterinary concerns regarding SO2 pollution are primarily over aquatic and wildlife health. One important exception relates to the use of unvented kerosene space heaters. Such heaters emit significant SO2 and associated acid aerosols. Total airborne concentrations can be exorbitant in closed-space situations. When SO2 gas is combined with other organic acid emissions, space heater emissions can cause ocular and respiratory irritation in animals and humans alike. Additionally, acid aerosol exposure from ambient SO2 pollution may occur in pets that are either housed outdoors or exercised outside for significant periods. Again, asthmatic humans are at particular risk (Bernstein et al, 2008); thus dogs and cats with chronic bronchial disease may be similarly susceptible to this irritant gas-particulate mixture.

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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Chapter 7: Respiratory Toxicants of Interest to Pet Owners

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