How exposure to environmental tobacco smoke, outdoor air pollutants, and increased pollen burdens influences the incidence of asthma

Environmental Health Perspectives, April, 2006 by M. Ian Gilmour, Maritta S. Jaakkola, Stephanie J. London, Andre E. Nel, Christine A. Rogers

Asthma is a multifactorial airway disease that arises from a relatively common genetic background interphased with exposures to allergens and airborne irritants. The rapid rise in asthma over the past three decades in Western societies has been attributed to numerous diverse factors, including increased awareness of the disease, altered lifestyle and activity patterns, and ill-defined changes in environmental exposures. It is well accepted that persons with asthma are more sensitive than persons without asthma to air pollutants such as cigarette smoke, traffic emissions, and photochemical smog components. It has also been demonstrated that exposure to a mix of allergens and irritants can at times promote the development phase (induction) of the disease. Experimental evidence suggests that complex organic molecules from diesel exhaust may act as allergic adjuvants through the production of oxidative stress in airway cells. It also seems that climate change is increasing the abundance of aeroallergens such as pollen, which may result in greater incidence or severity of allergic diseases. In this review we illustrate how environmental tobacco smoke, outdoor air pollution, and climate change may act as environmental risk factors for the development of asthma and provide mechanistic explanations for how some of these effects can occur. Key words: air pollution, asthma, cigarette smoke, climate change, diesel exhaust, environment, inflammation, mechanisms, ozone, particulate matter, pollen. doi: 10.1289/ehp.8380 available via http://dx.doi.org/[Online 26 January 2006]

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Allergic diseases are the sixth leading cause of chronic illness in the United States, affecting 17% of the population and costing the health care system about $18 billion annually [American Academy of Allergy, Asthma and Immunology (AAAAI) 2000]. Approximately 40 million Americans suffer from allergic rhinitis (hay fever), largely in response to common aeroallergens, resulting in 3.8 million lost days of work and school [Centers for Disease Control and Prevention (CDC) 2004]. Children with asthma are usually a subset of allergic individuals with more respiratory involvement characterized by chronic lung inflammation, airway hyperreactivity (AHR), and reversible airflow obstruction, whereas new asthma in adults may be more often non-allergic in nature [e.g., exercise-induced asthma (AAAAI 2000) and irritant-induced asthma (Tarlo 2003)]. Asthma commonly begins in childhood, but can also start in adulthood, and frequently requires doctor visits, long-term medication use, and in some cases hospitalizations. Currently, the CDC estimates the prevalence of asthma in the U.S. adult population to be 7.5% (16 million; CDC 2004).

Asthma and allergies have a strong hereditary and hence genetic component that likely works by modifying responses to ubiquitous environmental exposures. The factors affecting the onset of allergies and asthma are complex, and considerable attention has focused on the indoor environment [Institute of Medicine (IOM) 2000], as well as outdoor pollutant exposures (Peden 2003). Cigarette smoke and diesel exhaust particles (DEPs), in particular, have been shown to act synergistically with allergen exposure to enhance the severity of immune-mediated lung disease [California Environmental Protection Agency (California EPA) 1997; Diaz-Sanchez et al. 1997), and new evidence shows that ozone exposure and proximity to major roadways are associated with increased incidence of disease (Diaz-Sanchez et al. 2003; Heinrich and Wichmann 2004). In this review we illustrate how environmental tobacco smoke (ETS), outdoor air pollution, and climate change may act as environmental risk factors for the development of asthma and provide mechanistic explanations for how some of these effects can occur.

Environmental Tobacco Smoke

Exposure to ETS--or passive smoking or exposure to secondhand smoke--is defined as exposure of a (nonsmoking) person to tobacco combustion products from smoking by others (Jaakkola and Jaakkola 1997). The fetus can be exposed either by the mother's active smoking or by her exposure to ETS during pregnancy. The harmful substances of tobacco are then transferred across the placenta to the fetus.

Tobacco smoke contains more than 4,000 chemical substances, many of which are carcinogenic, mutagenic, irritating, or toxic. Exposure to ETS can be assessed by measuring air nicotine or respirable suspended particle concentrations with personal or stationary monitors (Jaakkola and Jaakkola 1997). Questionnaires are commonly used for assessing ETS exposure in health effects studies because they are relatively cheap and allow exposure assessment during different time periods and in different indoor environments. In addition, biomarkers can be measured as proxies for dose, including cotinine in body fluids and hair nicotine. Studies conducted in the United States and Europe have detected cotinine in urine as an indicator of passive smoking in > 80% of the nonsmoking populations (Pirkle et al. 1996; Riboli et al. 1990; reviewed by Jaakkola 2000). Questionnaire-based assessment of ETS exposure has varied from 7% in Finnish children (Jaakkola et al. 1994) to > 60% among Californian young adults (California EPA 1997).