The epidemiology and genetics of asthma risk associated with air pollution

doi:10.1016/j.jaci.2004.12.003

Journal of Allergy and Clinical Immunology

Volume 115, Issue 2, February 2005, Pages 213-219

https://doi.org/10.1016/j.jaci.2004.12.003 Get rights and content

The occurrence of asthma and allergic diseases has continued to increase in the United States and worldwide, despite general improvements in air quality over the past 40 years. This observation has led many to question whether air quality is truly a significant risk factor in the development and exacerbation of asthma and whether further improvement in air quality is likely to result in improved health outcomes. However, epidemiologic studies have shown that levels of pollutants of less than the current ambient air quality standards still result in exacerbations of asthma and are associated with other morbidities as well. Specific locations, such as living near a roadway, might pose a special exposure risk. Genetic factors almost certainly play a role in determining susceptibility to pollutants, such as including those involved with antioxidant defenses. The best studied of these in the context of air pollution risks are glutathione-S-transferase polymorphisms. Irrespective of whether pollutants contribute to the development of asthma or the well-documented increases in asthma results in more people having pollutant-induced disease, poor air quality in many places remains a significant problem for patients with asthma and allergic disease. A number of public health, pharmaceutical, and nutriceutical interventions might mitigate the effects of pollutant exposure and deserve further study.

Section snippets

Epidemiology of air pollutant exposure and asthma

Epidemiologic studies of the effect of air pollution have examined both the exacerbation of lung disease associated with acute exposure to pollutants and the development of lung disease or impairment associated with chronic pollutant exposure. Air pollutants implicated in these effects include those regulated by the US Environmental Protection Agency under the Clean Air Act, including nitrogen dioxide (NO₂), ozone, and particulate matter (PM; Table I),¹ as well as other agents, including

Genetics of air pollutant response

The immediate effect of air pollutants on airway function in both healthy and allergic persons has been extensively reviewed, and a full review can be found elsewhere.1, 2 However, in considering the genetics of response to pollutants, a brief review of the phenotypes of such responses is warranted. Ozone, NO₂, and PM (or various components of PM, including diesel exhaust particles and endotoxin) have all been shown to induce acute inflammatory responses in the airway and, in allergic persons,

Interventions (Table III)

Public health approaches to decrease air pollutants have been shown to have a measurable effect on health outcomes. One example of this occurred in concert with the 1996 Olympic Games held in Atlanta. Coincident with attempts by the local government to decrease ozone generation caused by vehicle exhaust, there was not only a decrease in summer ozone levels but also a significant decrease in asthma morbidity noted during this time.⁴⁴ Likewise, in Dublin, Ireland, a ban on bituminous coal sales

Future directions

Clearly much remains to be learned by using systems biologic, genomic, and epidemiologic approaches in examining in vivo, cellular, and population responses to pollutant stress. Antioxidants and regulators of inflammation are logical targets for investigation. Traditional therapy that decreases chronic allergic inflammation, such as inhaled corticosteroids, also protects allergic asthmatic subjects (but not healthy individuals) against the effect of challenge with air pollutants. Other

References (64)

J.A. Bernstein et al.
Health effects of air pollution
J Allergy Clin Immunol
(2004)
R. McConnell et al.
Asthma in exercising children exposed to ozone: a cohort study
Lancet
(2002)
A.J. Chauhan et al.
Personal exposure to nitrogen dioxide (NO2) and the severity of virus-induced asthma in children
Lancet
(2003)
M.C. White et al.
Exacerbations of childhood asthma and ozone pollution in Atlanta
Environ Res
(1994)
W.F. McDonnell et al.
Long-term ambient ozone concentration and the incidence of asthma in nonsmoking adults: the AHSMOG Study
Environ Res
(1999)
P.J. Gergen
Environmental tobacco smoke as a risk factor for respiratory disease in children
Respir Physiol
(2001)
S. Lin et al.
Childhood asthma hospitalization and residential exposure to state route traffic
Environ Res
(2002)
T.M. Bastain et al.
Intraindividual reproducibility of nasal allergic responses to diesel exhaust particles indicates a susceptible phenotype
Clin Immunol
(2003)
F.D. Gilliland et al.
Effect of glutathione-S-transferase M1 and P1 genotypes on xenobiotic enhancement of allergic responses: randomised, placebo-controlled crossover study
Lancet
(2004)
L. Clancy et al.
Effect of air-pollution control on death rates in Dublin, Ireland: an intervention study
Lancet
(2002)

G.E. Hatch

Asthma, inhaled oxidants, and dietary antioxidants

Am J Clin Nutr

(1995)

F.J. Kelly et al.

Altered lung antioxidant status in patients with mild asthma

Lancet

(1999)

D. Diaz-Sanchez et al.

Effect of topical fluticasone propionate on the mucosal allergic response induced by ragweed allergen and diesel exhaust particle challenge

Clin Immunol

(1999)

J.F. Trapp et al.

The effect of of glucocorticoids on grain dust-induced airway disease

Chest

(1998)

N.E. Alexis et al.

Blunting airway eosinophilic inflammation results in a decreased airway neutrophil response to inhaled LPS in patients with atopic asthma: a role for CD14

J Allergy Clin Immunol

(2001)

D.B. Peden

Air pollution: indoor and outdoor

R. McConnell et al.

Prospective study of air pollution and bronchitic symptoms in children with asthma

Am J Respir Crit Care Med

(2003)

R. McConnell et al.

Air pollution and bronchitic symptoms in Southern California children with asthma

Environ Health Perspect

(1999)

Committee of the Environmental and Occupational Health Assembly of the American Thoracic Society

Health effects of outdoor air pollution

Am J Respir Crit Care Med

(1996)

L. Dijkstra et al.

Respiratory health effects of the indoor environment in a population of Dutch children

Am Rev Respir Dis

(1990)

B. Brunekreef et al.

Indoor nitrogen dioxide exposure and children's pulmonary function

J Air Waste Manage Assoc

(1990)

L.M. Neas et al.

Association of indoor nitrogen dioxide with respiratory symptoms and pulmonary function in children

Am J Epidemiol

(1991)

R.T. van Strien et al.

Exposure to NO2 and nitrous acid and respiratory symptoms in the first year of life

Epidemiology

(2004)

R. McConnell et al.

Prospective study of air pollution and bronchitic symptoms in children with asthma

Am J Respir Crit Care Med

(2003)

I. Romieu et al.

Effects of urban air pollutants on emergency visits for childhood asthma in Mexico City

Am J Epidemiol

(1995)

I. Romieu et al.

Effects of air pollution on the respiratory health of asthmatic children living in Mexico City

Am J Respir Crit Care Med

(1996)

I. Romieu et al.

Effects of intermittent ozone exposure on peak expiratory flow and respiratory symptoms among asthmatic children in Mexico City

Arch Environ Health

(1997)

J.F. Gent et al.

Association of low-level ozone and fine particles with respiratory symptoms in children with asthma

JAMA

(2003)

R.J. Delfino et al.

Daily asthma severity in relation to personal ozone exposure and outdoor fungal spores

Am J Respir Crit Care Med

(1996)

C.A. Pope

Epidemiology of fine particulate air pollution and human health: biologic mechanisms and who's at risk?

Environ Health Perspect

(2000)

C.A. Pope

Respiratory hospital admissions associated with PM10 pollution in Utah, Salt Lake, and Cache Valleys

Arch Environ Health

(1991)

C.A. Pope

Respiratory disease associated with community air pollution and a steel mill, Utah Valley

Am J Public Health

(1989)

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Although the causes of asthma are inconclusive, it is fairly known that exposure to outdoor air pollutants can cause asthma, especially children's asthma morbidity. Whereas transportation is one of the major sectors that generate air pollutants, previous research that investigates the correlation between transportation and asthma narrowly focuses on the contribution of automobile traffic to children's asthma. Developing three spatial regression models (a spatial lag (SL) model, a spatial error (SE) model, and a general spatial (SAC) model), this paper investigates the roles of a variety of transportation factors in two distinct stages of children's asthma morbidity; asthma and severe asthma. With consideration to asthma-related socio-economic factors in the City of Seoul, the SE (R² = 0.31) and SAC (R² = 0.34) models consistently indicate that three out of four transportation factors associate with children's severe asthma at statistically significant level. They include the negative influence of bus transit and dense intersections, and the positive influence of active transportation activities on children's asthma severity. Interestingly, however, no significant contribution of transportation factors to children's asthma morbidity was identified by the SE (R² = 0.29) and SAC (R² = 0.28) models. Shedding more light on the complexity of children's asthma morbidity and severity, this paper proposes collaborative partnerships not only among multi- dimensional agencies, but also among multi-level government organizations.
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Citation Excerpt :
The WHO's international agency for research on cancer (IARC) classifies air pollution as a ‘Group 1’ carcinogen (IARC, 2013). Several epidemiological studies have previously shown that exposure to PM2.5 increases the risk for morbidity and mortality due to cardiopulmonary diseases (Pope et al., 2015; Brook et al., 2010; Pope and Dockery, 2006; Pope et al., 2004) as well as exacerbate the pre-existing medical conditions such as asthma, coronary obstructive pulmonary disease (COPD) (Peden, 2005; Sunyer et al., 2000) and other respiratory ailments especially among the elderly and children (Cançado et al., 2006). Also, from experimental studies exposure to PM2.5 has been shown to induce respiratory (Harkema et al., 2004; Morishita et al., 2004) and cardiovascular (Bagate et al., 2006; Watkinson et al., 2003) health outcomes and animals with pre-existing cardiopulmonary conditions are even more susceptible to adverse effects of exposure to PM2.5 (Wagner et al., 2012; Kang et al., 2002).
Health effects linked to PM_2.5, have been extensively studied in developed countries of Europe and N. America. However, little has been done in Saudi Arabia and the Middle East. This study evaluated the morbidity risk for cardiovascular (CVD) and respiratory (RD) diseases, associated with PM_2.5 exposure in Jeddah, Saudi Arabia. 24-h PM_2.5 sampling was conducted at 3 sites for 6 weeks quarterly from Apr 8th, 2013–Feb 18th, 2014 with simultaneous hospital data collection. The relative risks (RRs) for cardiopulmonary morbidity at different moving averages (MAs) of lagged exposures were estimated using a generalized linear time-series model. Elevated risks for RD were associated with recent PM_2.5 exposures (0–2 days). RD prevalence was highest in children 0–14 years. Overall, RD morbidity risk ranged from 1.081 (CI: 1.005–1.162) to 1.096 (CI: 1.023–1.173) at MAs_2–4; male, 1.081 (CI: 1.019–1.146) to 1.087 (CI: 1.020–1.159) at MAs_2–3, and female, 1.086 (CI: 1.007–1.172) to 1.093 (CI: 1.017–1.175) at MAs_2–4. Generally, females 0–14 years were the most at risk for RDs with RR = 1.097 (CI: 1.025–1.174) to 1.148 (CI: 1.049–1.257). CVD morbidity risk was highest in ER visits with overall RR = 1.057 (CI: 1.005–1.111) to 1.137 (CI: 1.065–1.213) across all MAs; male, 1.060 (CI: 1.007–1.204) to 1.131 (CI: 1.060–1.208); female, 1.065 (CI: 1.008–1.125) to 1.116 (CI: 1.045–1.192). PM_2.5 exposure showed significantly increased cardiopulmonary morbidity risk, accentuating the severe health effects associated with elevated PM_2.5 in Jeddah. Overall, females (0–14 years) were more at risk for RD morbidity than males. CVD morbidity risk was relatively higher in males than females, with highest risk observed in age-groups above 40 years.
Built environment factors contribute to asthma morbidity in older people: A case study of Seoul, Korea
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This paper aims to examine various built environment factors contributing to asthma and severe asthma morbidities in older people by performing spatial regression analysis. By controlling the socio-demographic factors of asthma in Seoul, we found a significant correlation of the built environment factors with severe asthma rather than with asthma in older people. The results suggest that population density and bus transit can make asthma severe in older people, while active transportation activities have a positive influence on severe asthma in older people. However, a significant contribution of built environment factors to asthma in older people is not identified. The findings from spatial regression imply that the collaboration of multi-level governments and agencies needs to develop policies for mitigating poor air quality from the perspective of environmental justice.
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Catalytic systems integrated in firewood stoves represent a potential secondary measure for emission reduction. However, the evaluation of catalytic efficiency is challenging since measurements, especially for PM emissions, upstream an integrated catalyst are not possible. Therefore, a special test facility, called “DemoCat”, was constructed which enabled parallel measurements in catalytically treated and untreated flue gas. The catalytic efficiency for CO, OGC and PM emissions was investigated under real-life operating conditions including ignition and preheating. The results confirmed a significant emission reduction potential (CO: > 95%, OGC: > 60%, PM: ∼30%). The conversion rates of CO and OGC emissions correlated with the space velocity and the coated area of honeycomb carriers which represent key parameters for the integration design. A quick response of the catalytic effect of around 5–12 min after ignition was observed when reaching 250 °C flue gas temperature at the catalyst. Most effective CO and OGC emission conversion was evident during the start-up and burn-out phase of a firewood batch. This reveals an important synergy for primary optimization which focuses particularly on the stretched intermediate phase of a combustion batch. The catalytic effect on PM emissions, especially on chemical composition, needs further investigations.
Long term durability and safety aspects of oxidizing honeycomb catalysts integrated in firewood stoves
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Critical heating operating conditions, as emulated in the safety test series, showed that temperatures below 400 °C at the integrated catalysts result in deposited agglomerations on the flow cross-section area of the catalyst's surface and in the risk of increased pressure drops. The deposited material of safety tests consisted predominantly of carbonaceous components with a share of around 120 g kg⁻¹ of OC and 280–450 g kg⁻¹ of EC. The oxidation potential of deposited carbonaceous material by higher temperatures was confirmed by a minor share of EC and OC (<50 g kg⁻¹) on the catalyst's surface when a heating cycle with five batches was performed. Concluding a sufficient heating-up of catalyst integrated stoves is necessary to avoid deposition of carbonaceous agglomerations.
The long term tests resulted in deposited agglomerations of mineral particles on the catalyst's surface of both types of catalysts. The metallic honeycomb catalyst was more sensitive regarding blocking which was indicated by total blocked cells and a significant increase of pressure drop by 5.3 Pa. Due to the effect of agglomerated particles gaseous emissions increased significantly (CO around 300%, OGC around 45%) whereas PM emissions were reduced by 63%. The regeneration of catalyst performance was almost completely achieved by cleaning the catalyst with water and pressured air. For processing of blocking the open diameter of cells of the honeycomb catalysts play a relevant role. Therefore, in terms of real-life applicability the ceramic honeycomb catalyst seems to be more suitable compared to the metallic honeycomb catalyst.

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(Supported by a grant from GlaxoSmithKline, Inc, Research Triangle Park, NC)

Series editor: Harold S. Nelson, MD

Disclosure of potential conflict of interest: David Peden has consultant arrangements with GlaxoSmithKline; has received grants–research support from the National Institutes of Health, the US Environmental Protection Agency, and GlaxoSmithKline; and is on the Speakers' Bureau for GlaxoSmithKline, AstraZeneca, and Merck.

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Review and feature articleThe epidemiology and genetics of asthma risk associated with air pollution

Section snippets

Epidemiology of air pollutant exposure and asthma

Genetics of air pollutant response

Interventions (Table III)

Future directions

J Allergy Clin Immunol

Lancet

Lancet

Environ Res

Environ Res

Respir Physiol

Environ Res

Clin Immunol

Lancet

Lancet

Am J Clin Nutr

Lancet

Clin Immunol

Chest

J Allergy Clin Immunol

Air pollution: indoor and outdoor

Prospective study of air pollution and bronchitic symptoms in children with asthma

Am J Respir Crit Care Med

Air pollution and bronchitic symptoms in Southern California children with asthma

Environ Health Perspect

Health effects of outdoor air pollution

Am J Respir Crit Care Med

Respiratory health effects of the indoor environment in a population of Dutch children

Am Rev Respir Dis

Indoor nitrogen dioxide exposure and children's pulmonary function

J Air Waste Manage Assoc

Association of indoor nitrogen dioxide with respiratory symptoms and pulmonary function in children

Am J Epidemiol

Exposure to NO2 and nitrous acid and respiratory symptoms in the first year of life

Epidemiology

Prospective study of air pollution and bronchitic symptoms in children with asthma

Am J Respir Crit Care Med

Effects of urban air pollutants on emergency visits for childhood asthma in Mexico City

Am J Epidemiol

Effects of air pollution on the respiratory health of asthmatic children living in Mexico City

Am J Respir Crit Care Med

Effects of intermittent ozone exposure on peak expiratory flow and respiratory symptoms among asthmatic children in Mexico City

Arch Environ Health

Association of low-level ozone and fine particles with respiratory symptoms in children with asthma

JAMA

Daily asthma severity in relation to personal ozone exposure and outdoor fungal spores

Am J Respir Crit Care Med

Epidemiology of fine particulate air pollution and human health: biologic mechanisms and who's at risk?

Environ Health Perspect

Respiratory hospital admissions associated with PM10 pollution in Utah, Salt Lake, and Cache Valleys

Arch Environ Health

Respiratory disease associated with community air pollution and a steel mill, Utah Valley

Am J Public Health

Review and feature article
The epidemiology and genetics of asthma risk associated with air pollution