Cervical cancerExposure to sunlight

Several ecological studies reported a reduced risk of cervical cancer incidence and/or mortality rate with respect to indices for solar ultraviolet-B (UVB) doses as a proxy for vitamin D production. These include one study in the United States that also used indices for smoking1, and two studies in China using latitude2 or annual solar UVB doses3.

A study looking at incidence of various cancers with respect to diagnosis of nonmelanoma skin cancer found a reduced risk of cervical cancer after correcting for smoking in each study4

A study of cancer incidence in an area (state) of Germany known for winegrowing found a trend of lower significantly reduced standardized incidence ratio (SIR) of cervical cancer as the fraction of land devoted to winegrowing increased while the SIR for skin cancer and melanoma increased slightly with increased fraction of land in winegrowing5. It was pointed out that this study found a beneficial effect of UVB in reducing the risk of cervical cancer in a study looking for the effects of pesticide use6

However, there is also evidence that risk of cervical cancer increases in summer. A study in the Netherlands investigated the seasonality of “cervical smears positive for HPV based on histopathologic epithelial changes pathognomonic of HPV” and found a peak in August7 8. By comparing the diagnosis rate with an index of sexual activity and conception, it was determined that the peak in August was not due to a higher rate of sexual activity that month. The study also found that during a 16-year period, “maximum HPV detection rate and maximum UV fluency are positively correlated (r=0.59, P The authors proposed that a “UV-mediated suppression of immune surveillance” was the cause of this peak.

A related explanation is that increased “release of nitric oxide from intracutaneous photolabile nitric oxide derivates9 by ultraviolet-A (UVA) (320–400 nm) changes the reaction to HPV. A laboratory study found: 

“Exposure of cells maintaining episomal high-risk HPV genomes to NO increased HPV early transcript levels 2- to 4-fold but did not increase viral DNA replication. Accompanying increased E6 and E7 mRNA levels were significant decreases in p53 and pRb protein levels, lower apoptotic indices, increased DNA double-strand breaks, and higher mutation frequencies when compared with HPV-negative cells10”.

The role of nitric oxide from UVA irradiance was proposed earlier as a factor for poorer prognosis for squamous cell carcinoma of the skin11.

Page last edited: 22 August 2011


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