Effect of low concentrations of ozone on inhaled allergen responses in asthmatic subjects

Molfino, N. A.; Wright, Stephanie; Katz, Ian; Tarlo, Susan M.; Silverman, Frances; McClean, Patricia; Szalai, J. P.; Raizenne, Mark; Slutsky, Arthur S.; Zamel, Noé

doi:10.1016/0140-6736(91)90346-q

Cited by 369 publications

(167 citation statements)

References 26 publications

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“…Irritant-induced induction of tachykinin release could serve to enhance ongoing inflammation in the asthmatic lung caused by known immune triggers. Examples consistent with this hypothetical mechanism include the putative interaction between ozone and pollen in asthma exacerbations (25), and the finding in subjects with mild asthma that airway responsiveness to inhaled allergen increases after ozone challenge (26). Airborne irritants could also indirectly enhance neuroinflammation by inhibition of neutral endopeptidase (NEP).…”

Section: Overview Of Asthma and Air Toxicsmentioning

confidence: 97%

Epidemiologic evidence for asthma and exposure to air toxics: linkages between occupational, indoor, and community air pollution research.

Delfino

2002

Environ Health Perspect

268

152

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Outdoor ambient air pollutant exposures in communities are relevant to the acute exacerbation and possibly the onset of asthma. However, the complexity of pollutant mixtures and etiologic heterogeneity of asthma has made it difficult to identify causal components in those mixtures. Occupational exposures associated with asthma may yield clues to causal components in ambient air pollution because such exposures are often identifiable as single-chemical agents (e.g., metal compounds). However, translating occupational to community exposure-response relationships is limited. Of the air toxics found to cause occupational asthma, only formaldehyde has been frequently investigated in epidemiologic studies of allergic respiratory responses to indoor air, where general consistency can be shown despite lower ambient exposures. The specific volatile organic compounds (VOCs) identified in association with occupational asthma are generally not the same as those in studies showing respiratory effects of VOC mixtures on nonoccupational adult and pediatric asthma. In addition, experimental evidence indicates that airborne polycyclic aromatic hydrocarbon (PAH) exposures linked to diesel exhaust particles (DEPs) have proinflammatory effects on airways, but there is insufficient supporting evidence from the occupational literature of effects of DEPs on asthma or lung function. In contrast, nonoccupational epidemiologic studies have frequently shown associations between allergic responses or asthma with exposures to ambient air pollutant mixtures with PAH components, including black smoke, high home or school traffic density (particularly truck traffic), and environmental tobacco smoke. Other particle-phase and gaseous co-pollutants are likely causal in these associations as well. Epidemiologic research on the relationship of both asthma onset and exacerbation to air pollution is needed to disentangle effects of air toxics from monitored criteria air pollutants such as particle mass. Community studies should focus on air toxics expected to have adverse respiratory effects based on biological mechanisms, particularly irritant and immunological pathways to asthma onset and exacerbation.

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Section: Overview Of Asthma and Air Toxicsmentioning

confidence: 97%

Epidemiologic evidence for asthma and exposure to air toxics: linkages between occupational, indoor, and community air pollution research.

Delfino

2002

Environ Health Perspect

268

152

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“…In the present study, only pollen count was available, and O 3 and pollen count had a synergistic effect on the risk of asthma attacks. Recent experimental studies have shown that O 3 may interact with air suspended allergens by amplifying the response to the allergen [29,30].…”

Section: Discussionmentioning

confidence: 99%

Short-term health effects of particulate and photochemical air pollution in asthmatic children

Just¹,

Ségala²,

Sahraoui³

et al. 2002

European Respiratory Journal

101

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In a previous panel study in Paris, France, detrimental effects of moderately high levels of winter air pollution on the symptoms and lung function of asthmatic children were demonstrated. A new study was conducted, with the aim of assessing the short-term effects of photo-oxidant and particulate air pollution on childhood asthma during spring and early summer in Paris.Eighty-two medically diagnosed asthmatic children were followed up for 3 months. Outcomes included the incidence and prevalence of asthma attacks, nocturnal cough, supplementary use of b 2 -agonists, symptoms of airway irritation, and peak expiratory flow (PEF) value and its variability. The statistical methods controlled for the lack of independence between daily health outcomes, temporal trends and pollen and weather conditions.Black smoke and nitrogen dioxide (NO 2 ) were associated with increases in the occurrence of nocturnal cough and respiratory infections. Ozone (O 3 ) was associated with an increase in the occurrence of asthma attacks and respiratory infections and with changes in lung function, as shown by an increase in PEF variability and a decrease in PEF. Statistically significant interactions were demonstrated between O 3 and temperature and between O 3 and pollen count for asthma attacks. O 3 levels had a greater effect on additional bronchodilator use and on irritations of the eyes, nose and throat on days on which no steroids were used. Particulate matter was associated with eye irritation only.This study showed that, although within international air quality standards, the prevailing levels of photo-oxidant and particulate pollution in spring and early summer had measurable short-term effects on children with mild-to-moderate asthma. Eur Respir J 2002; 20: 899-906 The short-term effects of air pollution in humans are predominantly assessed by means of time series studies. These recently reviewed [1] studies have shown broadly consistent associations between air pollutants and a number of related outcomes, such as total mortality, cardiorespiratory mortality and hospital admissions. To ensure that relationships observed are causal, it is necessary to check that studies with different designs show similar associations [2] and that there is coherence between a broad range of related health outcomes [3]. As recently reviewed [4,5], panel studies provide these advantages. The health effects are measured on an individual basis, whereas the exposure data are mostly based on aggregated data. These studies are often conducted on the most susceptible subgroups of the population, such as children and asthmatics. Previously, a panel study was conducted in Paris, France [6], in which the detrimental effect of moderately high levels of winter air pollution on the symptoms and lung function of asthmatic children was demonstrated. As attention is increasingly focused on photo-oxidant air pollution episodes, a new study was conducted with the aim of assessing the short-term effects of photo-oxidant and particulate pollution on the heal...

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“…Ozone has been of particular concern, as it provokes airway inflammation at very low levels (Aris et al 1993). In addition, ozone increases airway reactivity (Horstman et al 1990;Kreit et al 1989), and there is evidence to suggest that ozone may potentiate the effects of allergens (Molfino et al 1991). Ozone levels have been related to increases in asthma admissions and emergency room visits among children in Atlanta, Georgia (White et al 1994), New Jersey (Cody et al 1992), and Mexico City (Romieu et al 1995).…”

Section: Risks At Different Agesmentioning

confidence: 99%

Children's health and the environment: public health issues and challenges for risk assessment.

Landrigan

Kimmel

Correa

et al. 2004

Environ Health Perspect

364

206

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Infants and children are not little adults. They are uniquely vulnerable to environmental toxicants. To protect infants and children against toxicants, the National Research Council in 1993 called for development of an approach to risk assessment that considers children's unique patterns of exposure and their special vulnerabilities to pesticides. Many aspects of that call were codified into federal law in the Food Quality Protection Act (FQPA) of 1996. This report highlights the central elements needed for development of a child-protective approach to risk assessment: a) improved quantitative assessment of children's exposures at different life stages, from fetal life through adolescence, including acute and chronic exposures, exposures via multiple routes, and exposures to multiple agents; b) development of new approaches to toxicity testing of chemicals that can detect unanticipated and subtle outcomes and that evaluate experimental subjects over the entire life span from early exposure to natural death to replicate the human experience; c) development of new toxicodynamic and toxicokinetic models that account for the unique physiologic characteristics of infants and children; d) development of new approaches to assessment of outcomes, functional, organ, cellular and molecular, over the entire life span; these measures need to be incorporated into toxicity testing and into long-term prospective epidemiologic studies of children; and e) application of uncertainty and safety factors in risk assessment that specifically consider children's risks. Under FQPA, children are presumed more vulnerable to pesticides than adults unless evidence exists to the contrary. Uncertainty and safety factors that are protective of children must therefore be incorporated into risk assessment when data on developmental toxicity are lacking or when there is evidence of developmental toxicity. The adequate protection of children against toxic agents in the environment will require fundamental and far-reaching revisions of current approaches to toxicity testing and risk assessment.

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Effect of low concentrations of ozone on inhaled allergen responses in asthmatic subjects

Cited by 369 publications

References 26 publications

Epidemiologic evidence for asthma and exposure to air toxics: linkages between occupational, indoor, and community air pollution research.

Epidemiologic evidence for asthma and exposure to air toxics: linkages between occupational, indoor, and community air pollution research.

Short-term health effects of particulate and photochemical air pollution in asthmatic children

Children's health and the environment: public health issues and challenges for risk assessment.

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