The incidence of allergic diseases is increasing, and research on their epidemiology, pathophysiology, and the prevention of onset is urgently needed. The onset of allergic disease begins in infancy with atopic dermatitis and food allergy and develops into allergic asthma and allergic rhinitis in childhood; the process is defined as “atopic march”. Atopic march is caused by multiple immunological pathways, including allergen exposure, environmental pollutants, skin barrier dysfunction, type 2 inflammation, and oxidative stress, which promote the progression of atopic march. Using recent evidence, herein, we explain the involvement of allergic inflammatory conditions and oxidative stress in the process of atopic march, its epidemiology, and methods for prevention of onset.

Objectives: The number of studies investigating the health effects of long-term exposure to air pollution is increasing, however, most studies have been conducted in Western countries. The health status of Asian populations may be different to that of Western populations and may, therefore, respond differently to air pollution exposure. Therefore, we evaluated the health effects of long-term exposure to traffic-related air pollution in Shizuoka, Japan.Methods: Individual data were extracted from participants of an ongoing cohort study. A total of 14 001 older residents, who were randomly chosen from all 74 municipalities of Shizuoka, completed questionnaires and were followed from December 1999 to March 2006. Individual nitrogen dioxide exposure data, as an index for traffic-related exposure, were modelled using a land use regression model. We assigned participants an estimated concentration of nitrogen dioxide exposure during 2000–2006. We then estimated the adjusted HR and their CI for a 10 μg/m³increase in exposure to nitrogen dioxide for all-cause or cause-specific mortality.Results: The adjusted HR for all-cause mortality was 1.02 (95% CI 0.96 to 1.08). Regarding cause-specific mortality, the adjusted HR for cardiopulmonary mortality was 1.16 (95% CI 1.06 to 1.26); in particular the adjusted HR for ischaemic heart disease mortality was 1.27 (95% CI 1.02 to 1.58) and for pulmonary disease mortality it was 1.19 (95% CI 1.02 to 1.38). Furthermore, among non-smokers, a 10 μg/m³increase in nitrogen dioxide was associated with a higher risk for lung cancer mortality (HR 1.30, 95% CI 0.85 to 1.93).Conclusion: Long-term exposure to traffic-related air pollution, indexed by nitrogen dioxide concentration, increases the risk of cardiopulmonary mortality, even in a population with a relatively low body mass index and increases the risk of lung cancer mortality in non-smokers.

Background: It is well known that large-scale poisonings caused by methylmercury occurred in Japan (Minamata, in the 1950s) and Iraq. However, in contrast to Iraq, there have been few sound epidemiologic studies in Minamata. We evaluated the effect of methylmercury on neurologic signs using data from a 1971 population-based study. Methods: Villages in 3 areas were selected for study: the Minamata area (a high-exposure area), the Goshonoura area (a medium-exposure area), and the Ariake area (a low-exposure area). We used place of residence as the exposure indicator. We examined associations between methylmercury exposure and the following neurologic signs measured on clinical examination: paresthesia of whole body, paresthesia of extremities, paresthesia around the mouth, ataxia, dysarthria, tremors, and pathologic reflexes. Results: Total population was 1120 in the high-exposure villages, 1845 in the medium-exposure villages, and 1165 in the low-exposure villages. In the Minamata area, 87% (n=833) of the eligible population (age 10 years and older) participated in the 1971 investigations, in the Goshonoura area, 93% (n = 1450), and in the Ariake area, 77% (n = 755). Compared with subjects in the Ariake area, the subjects in the Minamata area manifested neurologic signs more frequently. The highest prevalence odds ratio was observed for paresthesia around the mouth (110; 95% confidence interval = 16–820). Although residents in the Goshonoura area had been exposed less heavily than those in the Minamata area, Goshonoura residents also had increased prevalence of neurologic signs. Conclusion: Long-term exposure to methylmercury has a strong adverse impact on neurologic signs among residents in a local community.