Developing Asthma in Childhood From Exposure to Secondhand Tobacco Smoke
Developing Asthma in Childhood From Exposure to Secondhand Tobacco Smoke
Objective: Studies have identified associations between household secondhand tobacco smoke (SHS) exposure and induction of childhood asthma. However, the true nature and strength of this association remains confounded in many studies, producing inconsistent evidence. To look for sources of potential bias and try to uncover consistent patterns of relative risk estimates (RRs) , we conducted a meta-analysis of studies published between 1970 and 2005.
Data sources: Through an extensive literature search, we identified 38 epidemiologic studies of SHS exposure and the development of childhood asthma (that also controlled for atopy history) from 300 potentially relevant articles.
Data synthesis: We observed substantial heterogeneity within initial summary RRs of 1.48 [95% confidence interval (CI) , 1.321.65], 1.25 (1.211.30) , and 1.21 (1.081.36) , for ever, current, and incident asthma, respectively. Lack of control for type of atopy history (familial or child) and child's own smoking status within studies and age category altered summary RRs in separate meta-regressions. After adjusting for these confounding characteristics, consistent patterns of association emerged between SHS exposure and childhood asthma induction. Our summary RR of 1.33 (95% CI, 1.141.56) from studies of incident asthma among older children (618 years of age) is 1.27 times the estimate from studies of younger children and higher than estimates reported in earlier meta-analyses.
Conclusions: This new finding indicates that exposure duration may be a more important factor in the induction of asthma than previously understood, and suggests that SHS could be a more fundamental and widespread cause of childhood asthma than some previous meta-analyses have indicated.
Asthma in childhood becomes a lifelong condition for many people, and there is evidence that its prevalence has increased over the past 50 years (Ross Anderson et al. 2007). Direct and indirect severe impacts on general health, well-being, and premature death can lead to large costs to the health care system for the management and treatment of asthma. The role of secondhand tobacco smoke (SHS) in asthma exacerbation is well accepted [U.S. Department of Health and Human Services (DHHS) 2006], whereas its role in childhood asthma induction is less well understood. Several reviews and meta-analyses have weighed the evidence of a causal relationship between exposure to SHS and the onset of asthma in children [Cook and Strachan 1999; Office of Environmental Health Hazard Assessment (OEHHA) 1997; Strachan and Cook 1998; U.S. DHHS 2006; U.S. Environmental Protection Agency (EPA) 1992].
These reviews and meta-analyses differ in their conclusions about the sufficiency of evidence to infer a causal relationship between SHS exposure and asthma induction in children. The U.S. EPA and California EPA concluded that SHS exposure is causally associated with an increase in the incidence of childhood asthma (OEHHA 1997; U.S. EPA 1992), based on studies of young children. Strachan and Cook (1998) observed elevated estimates of relative risk (RRs) from studies of preschool age and equivocal RRs from studies of older children. Their meta-analysis, originally conducted in the mid-1990s, was updated in the most recent Surgeon General's Report (SGR) on Health Effects from Involuntary Exposure to Tobacco Smoke (U.S. DHHS 2006). The SGR concluded that the evidence is suggestive, but not sufficient to infer a causal relationship between SHS and the induction of childhood asthma. The SGR's main reason for this conclusion is that the small number of studies that examined an association of SHS exposure from parental smoking with asthma incidence among older children (when there is reasonable diagnostic certainty) found inconsistent evidence of elevated RRs.
Many additional individual epidemiologic studies have been published since 2001 (the cutoff of Strachan and Cook's latest update in the SGR) (Gilliland et al. 2001; Hessel et al. 2001; Jaakkola et al. 2001; Kivity et al. 2001; Mannino et al. 2001; Pokharel et al. 2001; Sturm et al. 2004; Takamura et al. 2001). Several of these newer studies have reported that control for important confounding variables such as atopy history (family or child history of atopy), prenatal exposure to maternal smoking, and smoking status of older children can substantially alter RRs (Gilliland et al. 2001; Hessel et al. 2001; Jaakkola et al. 2001; Pokharel et al. 2001). Because atopy history was a particularly important confounder, we chose to conduct a meta-analysis of studies that controlled for atopy history. We examined the effects of other potentially confounding factors and study-wide characteristics on the summary RR of developing childhood asthma from exposure to household SHS to see whether consistent patterns of RRs emerge.
One of our goals was to use meta-regression on atopy-controlled studies to quantitatively explore the effects of these other potentially important sources of heterogeneity on the summary RR. Some of the heterogeneity among RRs reported in previous meta-analyses (Cook and Strachan 1999; Strachan and Cook 1998; U.S. DHHS 2006) may be related to uncontrolled confounding factors such as atopy history, age, sex, race, and the status of smoking in older study subjects. Other sources of heterogeneity among studies may include the age at which exposure and disease status are assessed, the assessment of maternal smoking versus other SHS sources, the evaluation of prenatal versus postnatal SHS exposure, the use of asthma incidence versus asthma prevalence as the outcome measure, the type of study design, or the subject recruitment source.
Our systematic review considered studies addressed in the meta-analyses of Cook and Strachan (1999), OEHHA (1997), Strachan and Cook (1998), and U.S. DHHS (2006). Our meta-analysis used the power provided by the more recent studies and the simultaneous examination of multiple characteristics through meta-regression to further examine the relationship between SHS exposure and induction of childhood asthma. We were particularly interested in the relationship between household SHS exposure and childhood asthma induction in older children.
Objective: Studies have identified associations between household secondhand tobacco smoke (SHS) exposure and induction of childhood asthma. However, the true nature and strength of this association remains confounded in many studies, producing inconsistent evidence. To look for sources of potential bias and try to uncover consistent patterns of relative risk estimates (RRs) , we conducted a meta-analysis of studies published between 1970 and 2005.
Data sources: Through an extensive literature search, we identified 38 epidemiologic studies of SHS exposure and the development of childhood asthma (that also controlled for atopy history) from 300 potentially relevant articles.
Data synthesis: We observed substantial heterogeneity within initial summary RRs of 1.48 [95% confidence interval (CI) , 1.321.65], 1.25 (1.211.30) , and 1.21 (1.081.36) , for ever, current, and incident asthma, respectively. Lack of control for type of atopy history (familial or child) and child's own smoking status within studies and age category altered summary RRs in separate meta-regressions. After adjusting for these confounding characteristics, consistent patterns of association emerged between SHS exposure and childhood asthma induction. Our summary RR of 1.33 (95% CI, 1.141.56) from studies of incident asthma among older children (618 years of age) is 1.27 times the estimate from studies of younger children and higher than estimates reported in earlier meta-analyses.
Conclusions: This new finding indicates that exposure duration may be a more important factor in the induction of asthma than previously understood, and suggests that SHS could be a more fundamental and widespread cause of childhood asthma than some previous meta-analyses have indicated.
Asthma in childhood becomes a lifelong condition for many people, and there is evidence that its prevalence has increased over the past 50 years (Ross Anderson et al. 2007). Direct and indirect severe impacts on general health, well-being, and premature death can lead to large costs to the health care system for the management and treatment of asthma. The role of secondhand tobacco smoke (SHS) in asthma exacerbation is well accepted [U.S. Department of Health and Human Services (DHHS) 2006], whereas its role in childhood asthma induction is less well understood. Several reviews and meta-analyses have weighed the evidence of a causal relationship between exposure to SHS and the onset of asthma in children [Cook and Strachan 1999; Office of Environmental Health Hazard Assessment (OEHHA) 1997; Strachan and Cook 1998; U.S. DHHS 2006; U.S. Environmental Protection Agency (EPA) 1992].
These reviews and meta-analyses differ in their conclusions about the sufficiency of evidence to infer a causal relationship between SHS exposure and asthma induction in children. The U.S. EPA and California EPA concluded that SHS exposure is causally associated with an increase in the incidence of childhood asthma (OEHHA 1997; U.S. EPA 1992), based on studies of young children. Strachan and Cook (1998) observed elevated estimates of relative risk (RRs) from studies of preschool age and equivocal RRs from studies of older children. Their meta-analysis, originally conducted in the mid-1990s, was updated in the most recent Surgeon General's Report (SGR) on Health Effects from Involuntary Exposure to Tobacco Smoke (U.S. DHHS 2006). The SGR concluded that the evidence is suggestive, but not sufficient to infer a causal relationship between SHS and the induction of childhood asthma. The SGR's main reason for this conclusion is that the small number of studies that examined an association of SHS exposure from parental smoking with asthma incidence among older children (when there is reasonable diagnostic certainty) found inconsistent evidence of elevated RRs.
Many additional individual epidemiologic studies have been published since 2001 (the cutoff of Strachan and Cook's latest update in the SGR) (Gilliland et al. 2001; Hessel et al. 2001; Jaakkola et al. 2001; Kivity et al. 2001; Mannino et al. 2001; Pokharel et al. 2001; Sturm et al. 2004; Takamura et al. 2001). Several of these newer studies have reported that control for important confounding variables such as atopy history (family or child history of atopy), prenatal exposure to maternal smoking, and smoking status of older children can substantially alter RRs (Gilliland et al. 2001; Hessel et al. 2001; Jaakkola et al. 2001; Pokharel et al. 2001). Because atopy history was a particularly important confounder, we chose to conduct a meta-analysis of studies that controlled for atopy history. We examined the effects of other potentially confounding factors and study-wide characteristics on the summary RR of developing childhood asthma from exposure to household SHS to see whether consistent patterns of RRs emerge.
One of our goals was to use meta-regression on atopy-controlled studies to quantitatively explore the effects of these other potentially important sources of heterogeneity on the summary RR. Some of the heterogeneity among RRs reported in previous meta-analyses (Cook and Strachan 1999; Strachan and Cook 1998; U.S. DHHS 2006) may be related to uncontrolled confounding factors such as atopy history, age, sex, race, and the status of smoking in older study subjects. Other sources of heterogeneity among studies may include the age at which exposure and disease status are assessed, the assessment of maternal smoking versus other SHS sources, the evaluation of prenatal versus postnatal SHS exposure, the use of asthma incidence versus asthma prevalence as the outcome measure, the type of study design, or the subject recruitment source.
Our systematic review considered studies addressed in the meta-analyses of Cook and Strachan (1999), OEHHA (1997), Strachan and Cook (1998), and U.S. DHHS (2006). Our meta-analysis used the power provided by the more recent studies and the simultaneous examination of multiple characteristics through meta-regression to further examine the relationship between SHS exposure and induction of childhood asthma. We were particularly interested in the relationship between household SHS exposure and childhood asthma induction in older children.
