Abstract

Background: In Japan, pollen counts increased between 1977 and 1987, including three peaks (1978- 1980, 1982, 1984-1986) coinciding with triphasic Kawasaki disease (KD) outbreaks. Epidemiological findings have been extensively accumulated that KD since 2003 and, from 2018 related specific intractable diseases such as systemic vasculitis, collagen diseases, inflammatory bowel diseases, idiopathic dilated cardiomyopathy and further from 2019 various cancers such as lung, breast, pancreatic, skin and kidney cancers may be correlated to pollen exposure (PE). Methods and results: To elucidate the effects of PE on occurrence of other cancers, we evaluated the annual occurrence of disorders in relation to pollen counts using data from a national database. Specifically, we evaluated the occurrence of uterine cancer, cervical cancer, corpus uteri cancer, prostate cancer, bladder cancer, stomach cancer, cancer of gallbladder and bile ducts (GBB), malignant lymphoma (ML), oral and pharyngeal cancer (o-phar. cancers), laryngeal cancer. During 1975–2015, the 1978-80 and 1984-1986 peaks of pollen scatter was the earliest big peaks with which simultaneous increase in occurrence of uterine, cervical, bladder, stomach, GBB, o-phar. cancers and laryngeal cancers. Furthermore, simultaneous outbreaks of each cancer coincided with subsequent ten peaks of pollen scatter till 2015. Our results showed statistically significant correlations for o-phar cancers, laryngeal, prostate and stomach cancers between the annual number of newly registered patients (nRPs) in the patient-registry year and annual pollen levels in the same patient-registry year. Significant correlations were also shown between the number of nRPs in the patient-registry year and annual pollen levels measured 1 year (GBB), 2 years (prostate), 3 years (corpus uteri, stomach, ML), 5 years (uterine), 6 years (uterine, corpus uteri, prostate, bladder, GBB), 7 years (o-phar, laryngeal) and, 9 and 16 years (cervical) before the patient-registry year. Conclusion: We assume that cumulative effects of PE in many cases within about 6 years and more before the diagnosis of cancers might possibly trigger onset of cancers when cumulative effects of PE as environmental stress overwhelmed immunoreactive threshold. The authors would like to discuss the triggering effect of PE (the action of PE to induce a carcinogenic state in humans) on humans as a compromised host, in the preliminary stages of cancer development, in which human papillomavirus is thought to be involved in the pathogenesis.

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