Introduction

Secondhand smoke (SHS) exposure remains a public health problem. Few, if any, studies include both children with and without asthma to assess differences in caregiver smoking behavior, risk perception, and SHS.

Methods

Participants were 738 daily U.S. smokers (443 caregivers of children with asthma [CG-AC] and 295 caregivers of healthy children [CG-HC]; 50.9% White, 25% Black, 15% Latino). Data are cross-sectional; SHS was measured through self-report and passive dosimetry.

Results

Compared with CG-HC, CG-AC had fewer risk factors for exposing children to SHS (lower nicotine dependence, higher motivation to quit, greater perceived benefits of cessation on child's health, and lower optimistic bias; all p values < .05). Specifically, 60.6% of CG-AC reported a household smoking ban versus 40.1% of CG-HC (p < .05), though >95% of both groups had detectable levels of SHS in their home. CG-AC self-reported lower SHS than CG-HC, but both groups had nearly equivalent SHS when measured objectively. CG-AC were almost twice as likely as CG-HC to report a home smoking ban when they had detectable levels of household SHS as measured by passive dosimetry (OR = 1.71; 95% CI = 1.2, 2.4; p = .003).

Conclusions

Caregivers of children with chronic health conditions, such as asthma, may be motivated to self-report lower levels of SHS. Child health status (e.g., asthma) may cue practitioners to inquire about SHS, but given the low proportion of household bans and high levels of actual exposure among both groups, SHS exposure assessment and reduction/elimination counseling should be prompted to occur for all children.

Objective

This study determined if secondhand smoke (SHS) exposure is related to asthma-related functional morbidity by examining racial/ethnic differences in non-Latino White (NLW), African American, and Latino families and whether racial/ethnic SHS exposure differences across families persist when accounting for smoking factors.

Methods

Participants were 305 caregiver smokers of children with asthma. Two passive dosimeters measured secondhand smoke: one in the home and one worn by the child.

Results

Higher SHS exposure was related to greater asthma-related functional morbidity. African Americans had higher levels of home SHS exposure than did Latinos (p = .003) or NLWs (p = .021). SHS exposure as assessed by the child-worn dosimeter did not differ across race/ethnicity. African American families were less likely to report a household smoking ban (46.4%) compared to Latinos (79.2%) and NLWs (67.9%; p < .05). African Americans were less likely to report having two or more smokers in the home (37.2%) compared to NLWs (53.6%; p < .05). NLWs reported the highest number of cigarettes smoked daily (Mdn = 15.00) compared to Latinos (Mdn = 10.00; p = .001) and African Americans (Mdn = 10.00; p < .001). SHS home exposure levels were regressed on race/ethnicity and relevant covariates. Household smoking ban (p < .001) and only one smoker in the home (p = .005) were associated with lower levels of SHS in the home; race/ethnicity was not significant.

Conclusions

Differences in SHS exposure across race/ethnicity exist among children with asthma, possibly due to differential presence of a household smoking ban and number of smokers in the home.

Aims

We tested two aims: (1) the teachable moment (TM): whether second-hand smoke exposure (SHSe) feedback motivates cessation in parents of children with asthma versus parents of healthy children (HC); and (2) whether greater intervention intensity [enhanced-precaution adoption model (PAM)] produces greater cessation than a previously tested intervention (PAM).

Design and interventions

Aim 1: two home visits (asthma education or child wellness), and cessation induction using motivational interviewing and SHSe feedback. Aim 2: post-home-visits, parents with asthmatic children were randomized to PAM (n = 171; six asthma education calls) or enhanced-PAM (n = 170; six asthma education/smoking cessation calls + repeat SHSe feedback).

Setting

Rhode Island, USA.

Participants

Parents of asthmatic (n = 341) or healthy (n = 219) children who did not have to want to quit smoking to enroll.

Measurements

Measurements were given at baseline, 2, 4, 6 and 12 months. Abstinence was bioverified. Outcomes were 7-day and 30-day point prevalence abstinence (ppa) and SHSe (primary) and asthma morbidity (secondary).

Findings

Aim 1: the TM was supported: parents of asthmatic children were more than twice as likely to achieve 30-day [odds ratio (OR) = 2.60, 95% confidence interval (CI) = 1.22-5.54] and 7-day ppa (OR = 2.26, 95% CI = 1.13-4.51) at 2 months (primary end-point) and have non-detectable levels of SHSe than HCs. Greater treatment intensity yielded stronger TM effects (OR = 3.60; 95% CI = 1.72-7.55). Aim 2: enhanced-PAM was more likely to achieve 30-day ppa at the primary end-point, 4 months (OR = 2.12, 95% CI 1.09-4.12) and improved asthma outcomes versus PAM.

Conclusions

Smoking cessation intervention (Motivational Interviewing plus biomarker feedback) appear to motivate smoking cessation more strongly among parents of asthmatic children than among parents of healthy children. Increased intervention intensity yields greater smoking cessation among parents of asthmatic children and better asthma outcomes.

Rationale

Stress is associated with asthma morbidity in Puerto Ricans (PRs), who have reduced bronchodilator response (BDR).

Objectives

To examine whether stress and/or a gene regulating anxiety (ADCYAP1R1) is associated with BDR in PR and non-PR children with asthma.

Methods

This was a cross-sectional study of stress and BDR (percent change in FEV1 after BD) in 234 PRs ages 9-14 years with asthma. We assessed child stress using the Checklist of Children's Distress Symptoms, and maternal stress using the Perceived Stress Scale. Replication analyses were conducted in two cohorts. Polymorphisms in ADCYAP1R1 were genotyped in our study and six replication studies. Multivariable models of stress and BDR were adjusted for age, sex, income, environmental tobacco smoke, and use of inhaled corticosteroids.

Measurements and main results

High child stress was associated with reduced BDR in three cohorts. PR children who were highly stressed (upper quartile, Checklist of Children's Distress Symptoms) and whose mothers had high stress (upper quartile, Perceived Stress Scale) had a BDR that was 10.2% (95% confidence interval, 6.1-14.2%) lower than children who had neither high stress nor a highly stressed mother. A polymorphism in ADCYAP1R1 (rs34548976) was associated with reduced BDR. This single-nucleotide polymorphism is associated with reduced expression of the gene for the β2-adrenergic receptor (ADRB2) in CD4(+) lymphocytes of subjects with asthma, and it affects brain connectivity of the amygdala and the insula (a biomarker of anxiety).

Conclusions

High child stress and an ADCYAP1R1 single-nucleotide polymorphism are associated with reduced BDR in children with asthma. This is likely caused by down-regulation of ADRB2 in highly stressed children.