Updated Science Articles
New information about asthma, medications, treatments, and triggers continues to emerge. One of the best places to search for new information is in the National Library of Medicine's PubMed (Medline) database.
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Pediatrics. 2008 Jun 16. [Epub ahead of print]
Wang C, Salam MT, Islam T, Wenten M, Gauderman WJ, Gilliland FD.
Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California.
OBJECTIVE. Associations between single-nucleotide polymorphisms in the beta2-adrenergic receptor gene and asthma and wheeze have been inconsistent. Recent studies indicated that tobacco smoke affects beta2-adrenergic receptor gene expression and associations of beta2-adrenergic receptor gene variants with asthma in adults. We aimed to investigate the joint effects of in utero and childhood secondhand tobacco smoke exposure and 2 well-characterized functional single-nucleotide polymorphisms (Arg16Gly and Glu27Gln) of beta2-adrenergic receptor gene on asthma and wheezing in 3128 non-Hispanic and Hispanic white children of the Children's Health Study. METHODS. We fitted logistic regression models to estimate odds ratios and 95% confidence intervals for the independent and joint effects of these single-nucleotide polymorphisms and in utero and secondhand tobacco smoke exposure on asthma and wheeze outcomes. RESULTS. Exposures to in utero maternal smoking and secondhand tobacco smoke were associated with wheezing. Children who were homozygous for the Arg16 allele and were exposed to maternal smoking in utero were at a threefold increased risk for lifetime wheeze compared with children who were unexposed and had at least 1 Gly16 allele. We found similar joint effects of secondhand tobacco smoke and Arg16Gly with wheezing. The risk for lifetime, current, and nocturnal wheeze increased with the number of smokers at home among Arg16 homozygous children. The results were consistent in 2 cohorts of children recruited in 1993 and 1996. Diplotype-based analyses were consistent with the single-nucleotide polymorphism-specific results. No associations were found for Glu27Gln. CONCLUSIONS. Both in utero and childhood exposure to tobacco smoke were associated with an increased risk for wheeze in children, and the risks were greater for children with the Arg16Arg genotype or 2 copies of the Arg16-Gln27 diplotype. Exposures to smoking need to be taken into account when evaluating the effects of beta2-adrenergic receptor gene variants on respiratory health outcomes.
J Asthma. 2008 May;45(4):325-32.
Lin S, Gomez MI, Hwang SA, Munsie JP, Fitzgerald EF.
New York State Department of Health, Bureau of Environmental and Occupational Epidemiology, Troy, New York 12180-2216, USA.
We present prevalence estimates of indoor and outdoor environmental risk factors for asthma from a cross-sectional study of children 1 to 17 years of age living in Buffalo, New York. A child's primary caretaker completed a questionnaire about the household's demographics, lifestyle habits, housing, indoor and outdoor environment, and the child's activity patterns, family history of asthma, asthma symptoms and treatment, and medical care access. Significant environmental risk factors were presence of smokers in the household, humidifier or vaporizer use, chemical odors indoors, frequent truck traffic, and chemical odors outdoors. Most of these risk factors can be mitigated or controlled.
Chest. 2008 Mar 13.
Farber HJ, Knowles SB, Brown NL, Caine L, Luna V, Qian Y, Lavori P, Wilson SR.
a. Section of Pediatric Pulmonology, Baylor College of Medicine, Houston, TX; b. Palo Alto Medical Foundation Research Institute, Palo Alto, CA; c. Department of Pediatrics, Kaiser Permanente Vallejo Medical Center, Vallejo, CA; d. Stanford University School of Medicine, Palo Alto, CA.
BACKGROUND Secondhand smoke triggers childhood asthma. Understanding sources, parental beliefs about, and readiness to change that exposure are important for designing smoke exposure reduction interventions. METHODS As part of screening for a clinical trial of a smoke exposure reduction intervention, 519 smoke-exposed children 3-12 years with asthma provided urine specimens for cotinine testing and their primary caregivers completed questionnaires. RESULTS The urine cotinine to creatinine ratio (CCR) was lowest if neither the primary caregiver nor day care provider smoked (mean CCR (standard deviation)=14.0 (14.4)), greater if either smoked (mean CCR (SD)=22.2 (21.3) and 26.3 (22.2) respectively), and greatest if both smoked (mean CCR (SD)=39.6 (27.5), p<0.01). Parental perception of their child's exposure was weakly associated with the child's CCR (r-square=0.11, p < 0.001). Most parents (58.3%) reported tobacco smoke exposure had small/no negative effect on their child's asthma. Substantial proportions of those for whom a specific exposure reduction action was relevant were classified as contemplating, preparing or had recently taken action to reduce their child's exposure, including smoking cessation (61.3%), keeping the child out of smoke-exposed places (72.7%), and making the child's home (49.2%) and non-home areas smoke-free (66.9%). CONCLUSIONS Smoking by the primary caregiver and day care provider are important sources of exposure for children with asthma. Parental assessment of their child's exposure is associated with biologically confirmed exposure, but cannot be relied upon to assess that exposure. Although the harm of smoke exposure was frequently underestimated, many parents appeared receptive to considering action to reduce their child's exposure. Clinical trial registered as NCT00217958 at clinicaltrials.gov.
J Asthma. 2007 Mar; 44(2):83-8.
Halterman JS, Fagnano M, Conn KM, Lynch KA, DelBalso MA, Chin NP
This study assessed knowledge regarding the harm of environmental tobacco smoke (ETS) exposure and barriers to reducing ETS from the point-of-view of urban parents of asthmatic children. We conducted in-depth interviews with 15 mothers of children with asthma. All parents had good knowledge regarding the harmful effects of ETS. While all children of smoking parents were exposed to ETS, parents described using various strategies to keep ETS away from children. Many parents experienced significant stress in their lives and used smoking to relieve their stress. Barriers to a smoke-free home included stress, addiction, and the use of ineffective strategies to reduce ETS exposure.
Curr Allergy Asthma Rep. 2007 Jul;7(4):303-9.
Exposure to environmental tobacco smoke (ETS) is a major source of indoor air pollution and causes adverse effects on the respiratory health of individuals with asthma. At least one third of children and adults with asthma are exposed to ETS on a regular basis. There is convincing evidence for a causal relationship between exposure to ETS and development of asthma in children and in nonsmoking adults. Exposure to ETS also worsens asthma control in children and nonsmoking adults who have established asthma. The mechanism by which ETS causes these harmful effects is not established but may involve genetic predisposition, impairment of lung development, and altered lung inflammatory responses. Workplace smoking restrictions and reduced smoking in the home may lower the prevalence of asthma, improve asthma control, and reduce the use of medical services in both children and adults who are exposed to ETS.
Environ Health Perspect. 2007 Jun;115(6):976-82. Epub 2007 Jan 25.
Jacobs DE, Kelly T, Sobolewski J.
We describe the successes and challenges faced by federal and local government agencies in the United States as they have attempted in recent years to connect public and environmental health, housing, community development, and building design with environmental, housing, and building laws, codes, and policies. These policies can either contribute to or adversely affect human physical and mental health, with important implications for economic viability, research, policy development, and overall social stability and progress. Policy impediments include tension between housing affordability and health investment that causes inefficient cost-shifting, privacy issues, unclear statutory authority, and resulting gaps in responsibility for housing, indoor air, and the built environment. We contrast this with other environmental frameworks such as ambient air and water quality statutes where the concept of "shared commons" and the "polluter pays" is more robust. The U.S. experiences in childhood lead poisoning prevention, indoor air, and mold provide useful policy insights. Local programs can effectively build healthy homes capacity through local laws and housing codes. The experience of coordinating remediation for mold, asthma triggers, weatherization, and other healthy housing improvements in Cuyahoga County, Ohio, is highlighted. The U.S. experience shows that policymakers should adopt a prevention-oriented, comprehensive multi-disciplinary approach at all levels of government to prevent unhealthy buildings, houses, and communities.
Environ Health Perspect. 2007 Jun;115(6):971-5. Epub 2007 Jan 25.
Wu F, Takaro TK.
BACKGROUND: Contaminants encountered in many households, such as environmental tobacco smoke, house dust mite, cockroach, cat and dog dander, and mold, are risk factors in asthma. Young children are a particularly vulnerable subpopulation for environmentally mediated asthma, and the economic burden associated with this disease is substantial. Certain mechanical interventions are effective both in reducing allergen loads in the home and in improving asthmatic children's respiratory health. RESULTS: Combinations of interventions including the use of dust mite-impermeable bedding covers, improved cleaning practices, high-efficiency particulate air vacuum cleaners, mechanical ventilation, and parental education are associated with both asthma trigger reduction and improved health outcomes for asthmatic children. Compared with valuated health benefits, these combinations of interventions have proven cost effective in studies that have employed them. Education alone has not proven effective in changing parental behaviors such as smoking in the home. CONCLUSIONS: Future research should focus on improving the effectiveness of education on home asthma triggers, and understanding long-term children's health effects of the interventions that have proven effective in reducing asthma triggers.
Pediatr Clin North Am. 2007 Feb;54(1):103-20, ix.
Sharma HP, Hansel NN, Matsui E, Diette GB, Eggleston P, Breysse P.
The burden of asthma for children in the United States is substantial and has continued to rise for the past 2 decades. There is growing evidence that the indoor environment may play an important role in the pathogenesis of childhood asthma. This article first reviews the effects of indoor allergen exposure and sensitization on asthma incidence and morbidity, focusing on dust mite, cockroach, pet, and rodent allergens. It then addresses the effects of indoor air pollutants (ozone, particulate matter, nitrogen dioxide, environmental tobacco smoke, sulfur dioxide, and carbon monoxide) on asthma morbidity.
Policy Brief UCLA Cent Health Policy Res. 2007 Feb;(PB2007-2):1-7.
Hastert TA, Babey SH, Brown ER, Meng YY.
Many Californians with asthma are exposed to environmental conditions in the home-such as the presence of tobacco smoke and furry pets-which can trigger asthma symptoms. In addition, many who have not been diagnosed with asthma experience asthma-like breathing problems when exposed to these same indoor conditions. Nearly 1.9 million California adults and 890,000 children have active asthma (7.3% of all adults and 10.4% of all children). Among those with active asthma, 970,000 adults and 300,000 children suffered from symptoms at least monthly in 2003. An additional 2.6 million California adults and 810,000 children who had not been diagnosed with asthma suffered from asthma-like symptoms such as wheezing in 2003 (11.1% of all adults and 9.3% of all children). A Publication of the UCLA Center for Health Policy Research Using results from the 2003 California Health Interview Survey (CHIS 2003), this policy brief examines the association of asthma symptoms and asthma-like breathing problems with smoking and the presence of tobacco smoke in the home, and with the presence of dogs and cats in the home. This brief presents the prevalence of monthly asthma symptoms among adults and children with active asthma and the prevalence of wheezing and other asthma-like symptoms in the previous year among those not diagnosed with asthma. Active asthma refers to being diagnosed with asthma and also reporting that one still has asthma and/or that one experienced an asthma attack in the past year. There are a number of known environmental triggers in the home, including environmental tobacco smoke, animal dander, dust mites, cockroaches, molds and pollens. This brief discusses those triggers for which CHIS 2003 collected useful data. Other triggers have also been found to significantly contribute to breathing problems.