The effect of cigarette smoke from the mother on bronchial responsiveness and severity of symptoms in children with asthma

Murray, Andrew B.; Morrison, Brenda J.

doi:10.1016/0091-6749(86)90348-9

Cited by 186 publications

(72 citation statements)

References 19 publications

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“…This association is consistent with a previously reported association in children between second-hand smoke exposure and increased asthma severity (19), which would be expected to result in less stability of symptoms and increased medication needs. Possibly supporting this, we found that case patients were more likely than controls to be receiving regular inhaled steroid medications at entry into the panel study, before the case-control component to the study (Table 1).…”

Section: Discussionsupporting

confidence: 82%

A Case‐Control Study of the Role of Cold Symptoms and other Historical Triggering Factors in Asthma Exacerbations

Tarlo

Broder

Corey

et al. 2000

Canadian Respiratory Journal

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BACKGROUND: Asthma exacerbations can be provoked by many triggers such as allergens, respiratory irritants and viral infections. The relative importance of these has not been prospectively documented in a case-control study. OBJECTIVE: To assess the relative importance of colds and other nonclimatic historical triggers of asthma exacerbations. METHODS: One hundred and nineteen adults and children with asthma in two Canadian cities participated in a one-year study of the role of exacerbating factors in asthma. Among these, 36 pairs (21 adult, 15 children) completed the casecontrol study. Patients were considered cases if they developed an acute asthma exacerbation and notified the centre within 24 h to allow the completion of a questionnaire and viral studies (cultures of nasopharyngeal swabs and serology). Control people with asthma were matched for sex, age and area of residence, had no exacerbation during the preceding four weeks and participated within 48 h of the case patients.

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Section: Discussionsupporting

confidence: 82%

A Case‐Control Study of the Role of Cold Symptoms and other Historical Triggering Factors in Asthma Exacerbations

Tarlo

Broder

Corey

et al. 2000

Canadian Respiratory Journal

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“…Asthma may be exacerbated by damp [44,45] or mouldy [46] housing conditions, although the evidence is not conclusive [47]. Smoking and passive exposure to cigarette smoke in the home is more common among people in lower income groups [13,48], and may increase the morbidity among asthmatics [49]. Although parental smoking has not been shown to increase the risk of hospital admissions for acute asthma in children [50,51], it is possible that smoking may contribute to the relationship found in this study.…”

Section: Discussionmentioning

confidence: 99%

The relationship between asthma admission rates, routes of admission, and socioeconomic deprivation

Watson¹,

Cowen²,

Lewis³

1996

Eur Respir J

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T Th he e r re el la at ti io on ns sh hi ip p b be et tw we ee en n a as st th hm ma a a ad dm mi is ss si io on n r ra at te es s, , r ro ou ut te es s o of f a ad dm mi is ss si io on n, , a an nd d s so oc ci io oe ec co on no om mi ic c d de ep pr ri iv va at ti io on n ABSTRACT: This study aimed to explore the relationship between hospital admissions for asthma and socioeconomic deprivation. A retrospective study examined one year of hospital admissions for asthma in the West Midlands region of England (n=10,044), and in one of the region's wealthier districts, Worcester (n=251). Age standardized admission ratios (SARs) for asthma, and the routes of hospital admission, were compared with the Townsend Deprivation Index for the place of residence.Asthma SAR was strongly associated with deprivation as measured by the Townsend Index for the district of residence (Spearman rank correlation coefficient ρ=0.65; p=0.004). Asthma admission rates for all age groups, except those aged over 65 yrs, were higher in poorer districts. A significantly greater proportion of emergency admissions in poorer districts came via Accident and Emergency departments, rather than general practitioner referrals (ρ=0.76; p<0.001). Within Worcester District, SAR was associated with Townsend Index for the ward of residence (ρ=0.39; p<0.001). This remained significant after excluding repeat admissions (ρ=0.45; p<0.001).We conclude that asthma admissions are strongly associated with deprivation in the community. Differences in the health care received during acute exacerbations by asthma patients from different economic backgrounds is likely to be an important factor in this relationship.

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“…Cigarette smoke is associated with a high risk of developing chronic bronchitis (1,2). Furthermore, cigarette smoke causes an increase in airway resistance in normal volunteers (3) and bronchial hyperresponsiveness in chronic active or passive smokers (4,5), and exacerbates symptoms ofasthma in children whose parents are smokers (6,7). Therefore, knowledge of the mechanisms of cigarette smoke-induced inflammation in the airways is important in relating smoking to the pathophysiology of disease.…”

Section: Introductionmentioning

confidence: 99%

Cigarette smoke induces bronchoconstrictor hyperresponsiveness to substance P and inactivates airway neutral endopeptidase in the guinea pig. Possible role of free radicals.

Dusser

Djokic²,

Borson³

et al. 1989

J. Clin. Invest.

215

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We examined the effects of acute exposure to cigarette smoke on the airway responses to substance P in anesthetized guinea pigs and on the activity of airway neutral endopeptidase (NEP). After exposure to air or to cigarette smoke we measured the change in total pulmonary resistance (RL) induced by increasing concentrations of aerosolized substance P in the absence or presence of the NEP inhibitor phosphoramidon. In the absence of phosphoramidon the bronchoconstrictor responses to substance P were greater in cigarette smoke-exposed guinea pigs than in air-exposed animals. Phosphoramidon did not further potentiate the responses to substance P in smoke-exposed guinea pigs, whereas it did so in air-exposed animals. In the presence of phosphoramidon, bronchoconstrictor responses to substance P in animals exposed to air or to cigarette smoke were not different. Aerosols of SOD delivered before cigarette smoke exposures dramatically reduced smoke-induced hyperresponsiveness to substance P, whereas heat-inactivated SOD had no effect on smoke-induced hyperresponsiveness to substance P. Cigarette smoke solution inhibited NEP activity from tracheal homogenate in a concentration-dependent fashion, an inhibitory effect that was mostly due to the gas phase of the smoke, but not to nicotine. The mild chemical oxidant N-chlorosuccinimide mimicked the concentration-dependent inhibitory effect of smoke solution on airway NEP activity. We conclude that cigarette smoke causes enhanced airway responsiveness to substance P in vivo by inactivating airway NEP. We suggest that cigarette smoke-induced inhibition of airway NEP is due to effects of free radicals.

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The effect of cigarette smoke from the mother on bronchial responsiveness and severity of symptoms in children with asthma

Cited by 186 publications

References 19 publications

A Case‐Control Study of the Role of Cold Symptoms and other Historical Triggering Factors in Asthma Exacerbations

A Case‐Control Study of the Role of Cold Symptoms and other Historical Triggering Factors in Asthma Exacerbations

The relationship between asthma admission rates, routes of admission, and socioeconomic deprivation

Cigarette smoke induces bronchoconstrictor hyperresponsiveness to substance P and inactivates airway neutral endopeptidase in the guinea pig. Possible role of free radicals.

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