Shenzhen Center for Chronic Disease Control, Shenzhen Institute of Dermatology, Shenzhen City, Guangdong Province, China.
Department of Nutrition and Food Hygiene, Hubei Key Laboratory of Food Nutrition and Safety, Ministry of Education Key Laboratory of Environment and Health and MOE Key Lab of Environment and Health, Key Laboratory of Environment and Health (Wuhan), Ministry of Environmental Protection, State Key Laboratory of Environment Health (Incubation), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan.
J Glob Health. 2024 Aug 6;14:04139. doi: 10.7189/jogh.14.04139.
Genetic and environmental factors contribute to psoriasis, but the impact of residential environments on this condition remains uncertain. We aimed to investigate the association of residential environments with psoriasis risk and explore its interaction with genes.
We retrieved data on the spatial distribution of residential environments at 300 and 1000 m buffer zones from the UK Biobank, including the proportions of natural environments, domestic gardens, green spaces, and blue spaces within these zones. We then used Cox hazard models to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs) for the associations between residential environments and psoriasis risk. Lastly, we constructed polygenic risk scores to determine genetic susceptibility and further analyse the interaction with residential environments.
Overall, 3755 incident cases of psoriasis were documented during a median follow-up of 12.45 years. Compared with the lowest exposure quantile (Q1), Q4 exposure to natural environments (1000 m buffer: HR = 1.16, 95% CI = 1.05-1.29; 300 m buffer: HR = 1.12, 95% CI = 1.02-1.24) and green spaces (1000 m buffer: HR = 1.16, 95% CI = 1.04-1.28; 300m buffer: HR = 1.10, 95% CI = 1.00-1.21) increased the risk of psoriasis, while Q4 exposure to domestic gardens (1000 m buffer: HR = 0.85, 95% CI = 0.77-0.93; 300m buffer: HR = 0.91, 95% CI = 0.83-1.00) and Q3 exposure to blue spaces (1000 m buffer: HR = 0.89, 95% CI = 0.81-0.98) were negatively associated with psoriasis risk. Among participants with a high genetic risk, those exposed to high levels of natural environments (1000 m buffer: HR = 1.49, 95% CI = 1.15-1.93; 300 m buffer: HR = 1.39, 95% CI = 1.10-1.77) and green spaces (300 m buffer: HR = 1.30, 95% CI = 1.04-1.64) had a higher risk of psoriasis, while those exposed to blue spaces (1000 m buffer: HR = 0.78, 95% CI = 0.63-0.98) had a lower risk of psoriasis. We also observed joint effects of genetic risk and residential environments and an antagonistic additive interaction between blue spaces and genetic risk (P = 0.011).
We observed that residing in natural environments and green areas increased the risk of psoriasis in our sample, while proximity to blue spaces and domestic gardens was associated to reduced risks. The association of residential environments with psoriasis risk was modified by genetic susceptibility.
遗传和环境因素都会导致银屑病，但居住环境对这种疾病的影响仍不确定。我们旨在调查居住环境与银屑病风险之间的关联，并探讨其与基因的相互作用。
我们从英国生物库中检索了居住环境在 300 米和 1000 米缓冲区的空间分布数据，包括这些区域内自然环境、私人花园、绿地和蓝区的比例。然后，我们使用 Cox 风险模型估计了居住环境与银屑病风险之间的关联的风险比 (HR) 和 95%置信区间 (CI)。最后，我们构建了多基因风险评分，以确定遗传易感性，并进一步分析与居住环境的相互作用。
在中位随访 12.45 年期间，共记录了 3755 例银屑病新发病例。与最低暴露定量 (Q1) 相比，Q4 暴露于自然环境 (1000 米缓冲区：HR=1.16，95%CI=1.05-1.29；300 米缓冲区：HR=1.12，95%CI=1.02-1.24) 和绿地 (1000 米缓冲区：HR=1.16，95%CI=1.04-1.28；300m 缓冲区：HR=1.10，95%CI=1.00-1.21) 增加了银屑病的风险，而 Q4 暴露于私人花园 (1000 米缓冲区：HR=0.85，95%CI=0.77-0.93；300m 缓冲区：HR=0.91，95%CI=0.83-1.00) 和 Q3 暴露于蓝区 (1000 米缓冲区：HR=0.89，95%CI=0.81-0.98) 与银屑病风险呈负相关。在具有高遗传风险的参与者中，那些暴露于高水平自然环境 (1000 米缓冲区：HR=1.49，95%CI=1.15-1.93；300 米缓冲区：HR=1.39，95%CI=1.10-1.77) 和绿地 (300 米缓冲区：HR=1.30，95%CI=1.04-1.64) 的人患银屑病的风险更高，而暴露于蓝区的人 (1000 米缓冲区：HR=0.78，95%CI=0.63-0.98) 患银屑病的风险更低。我们还观察到遗传风险和居住环境的联合效应，以及蓝区和遗传风险之间拮抗的加性相互作用 (P=0.011)。
我们发现，在我们的样本中，居住在自然环境和绿地中会增加患银屑病的风险，而接近蓝区和私人花园与降低风险有关。居住环境与银屑病风险之间的关联受到遗传易感性的影响。
