家长的压力水平与儿童哮喘成正比
支气管哮喘是最常见的儿童疾病之一。儿童吸入的微粒物质可能引发呼吸道炎症。当遇到诱发因素,这些炎症细胞就可能会释放多种炎症介质和细胞因子,引起哮喘。对于哮喘的诱因,人们已可以列出一张清单:遗传、环境污染、过敏、剧烈运动、天气等。美国加利福尼亚南部大学的一项研究为这张清单添加了一项内容:家长的紧张情绪和压力。这项研究成果发表在《美国国家科学院学报》(PNAS)上。
加利福尼亚南部大学研究人员观察研究约2500名年龄在5岁到9岁的非哮喘患儿。研究结果显示,家长的压力水平与儿童对普通哮喘诱因的抵御能力密切相关。在同等外部环境的条件下,如果家长“紧张,有压力”,他们的孩子患哮喘机率比其它儿童高50%。不过,“家长压力重”这一单一因素不会增加患病风险。但当它与其他诱因,如周围环境污染严重或吸入“二手烟”相结合就足以诱发哮喘。参与这项研究罗布·麦康奈尔说:“哮喘是一种复杂的疾病,可能有多种诱因。这项研究成果为我们理解疾病诱因提供了一个线索。”
PNAS July 20, 2009, doi: 10.1073/pnas.0812910106
Parental stress increases the effect of traffic-related air pollution on childhood asthma incidence
Ketan Shankardassa, Rob McConnellb,1, Michael Jerrettc, Joel Milamb, Jean Richardsonb and Kiros Berhaneb
aCentre for Research on Inner City Health, The Li Ka Shing Knowledge Institute of St. Michael’s Hospital, 30 Bond Street, Toronto, ON, Canada M5B 1W8;
bDepartment of Preventive Medicine, Keck School of Medicine, University of Southern California, 1540 Alcazar Street, Suite 236, Los Angeles, CA 90089-9013; and
cSchool of Public Health, Division of Environmental Health Science, University of California, Berkeley, 50 University Hall #7360, Berkeley, CA 94720-7360
Exposure to traffic-related pollution (TRP) and tobacco smoke have been associated with new onset asthma in children. Psychosocial stress-related susceptibility has been proposed to explain social disparities in asthma. We investigated whether low socioeconomic status (SES) or high parental stress modified the effect of TRP and in utero tobacco smoke exposure on new onset asthma. We identified 2,497 children aged 5–9 years with no history of asthma or wheeze at study entry (2002–2003) into the Children’s Health Study, a prospective cohort study in southern California. The primary outcome was parental report of doctor-diagnosed new onset asthma during 3 years of follow-up. Residential exposure to TRP was assessed using a line source dispersion model. Information about maternal smoking during pregnancy, parental education (a proxy for SES), and parental stress were collected in the study baseline questionnaire. The risk of asthma attributable to TRP was significantly higher for subjects with high parental stress (HR 1.51 across the interquartile range for TRP; 95% CI 1.16–1.96) than for subjects with low parental stress (HR 1.05, 95% CI 0.74–1.49; interaction P value 0.05). Stress also was associated with larger effects of in utero tobacco smoke. A similar pattern of increased risk of asthma was observed among children from low SES families who also were exposed to either TRP or in utero tobacco smoke. These results suggest that children from stressful households are more susceptible to the effects of TRP and in utero tobacco smoke on the development of asthma.

