Monitoring of urinary iodine concentration in naval pilots: should iodine be supplemented or limited at coastal stations?

Background Airline crew are exposed to ionizing radiation as part of their occupation and have a documented increased risk of melanoma and cataracts. However, whether their occupation predisposes them to an increased risk of thyroid cancer is not established. The purpose of this systematic review and meta-analysis was to assess the risk of thyroid cancer in airline cockpit and cabin crew compared with the general population. Methods The MEDLINE database accessed via PubMed and Cochrane Database were searched. We included cohort studies reporting the standardized incidence ratio (SIR) or standardized mortality ratio (SMR) of thyroid cancers in any flight-based occupation. Results Of the 1777 citations retrieved in PubMed, eight studies with a total of 243,088 aircrew members and over 3,334,114 person-years of follow-up were included in this meta-analysis. No relevant studies were identified on Cochrane Database. The overall summary SIR of participants in any flight-based occupation was 1.11 (95% CI, 0.79–1.57; p = 0.613; 6 records). The summary SIR for cockpit crew was 1.21 (95% CI, 0.75–1.95; p = 0.383; 4 records) and the summary SIR for cabin crew was 1.00 (95% CI, 0.60–1.66; p = 0.646; 2 records). The overall summary standardized mortality ratio for airline crew was 1.19 (95% CI, 0.59–2.39; p = 0.773; 2 records). Conclusion Airline crew were not found to have a significantly elevated risk of thyroid cancer incidence or mortality relative to the general population. Future research should capitalize on the growing occupational cohort dataset and employ innovative methods to quantify lifetime radiation exposure to further assess thyroid cancer risk in airline crew. Electronic supplementary material The online version of this article (10.1186/s41199-018-0034-8) contains supplementary material, which is available to authorized users.

Background The effect of iodine on papillary thyroid cancer (PTC) has been controversial for many years. Since urinary iodine is an effective indicator of iodine intake, some recent epidemiological studies have described the relationship between urinary iodine concentration (UIC) and PTC. Methods We searched PubMed, Embase, Cochrane Library, and Web of Science for case-control studies about UIC and PTC published before September 2022. Results are presented as the overall odds ratio (OR) and 95% confidence intervals (CI). Results According to the analysis of the included studies, excessive iodine intake (UIC≥300ug/L) was positively associated with the occurrence of PTC patients compared with healthy controls (OR4.05, 95%CI 1.64-10.02, P=0.002). Meanwhile, adequate iodine exposure (100≤UIC<200ug/L) may play a protective role in the occurrence of PTC compared with healthy individuals (OR 0.36, 95%CI 0.14-0.91, P=0.03) while the difference in the prevalence of insufficient iodine intake (UIC<100ug/L) and iodine above requirements (200≤UIC<300ug/L) among the two groups were not significant (deficiency: OR 0.38, 95%CI 0.13-1.16, P=0.09; above requirements: OR 0.92, 95%CI 0.40-2.10, P=0.84). After comparing the UIC levels of PTC patients with those of other thyroid diseases, we found that there was also no significant difference in the incidence of different levels of UIC in the two groups (excessive: OR 1.25, 95%CI 0.87-1.80, P=0.22; above requirements: OR 0.93, 95%CI 0.77-1.14, P=0.49; adequate: OR 0.96, 95%CI 0.78-1.17, P=0.67; deficiency: OR 1.02, 95%CI 0.86-1.22, P=0.80). The result of this meta-analysis also did not support the relationship between UIC and the BRAF mutation and lymph node metastasis (LNM) of PTC patients. Besides, we also found that studies on the relationship between urinary iodine and PTC may be influenced by the way UIC was measured. Conclusion The 10 case-control included studies involved a total of 6,544 participants. The results of this meta-analysis showed excessive iodine intake, that is, UIC≥300ug/L was associated with the occurrence of PTC but not with BRAF mutation and LNM while adequate iodine intake (100≤UIC<200ug/L) may be one of the protective factors for PTC.

The activity of the hypothalamic-pituitary-thyroid (HPT) axis is rapidly adjusted by energy balance alterations. Glucocorticoids can interfere with this activity, although the timing of this interaction is unknown. In vitro studies indicate that, albeit incubation with either glucocorticoid receptor (GR) agonists or protein kinase A (PKA) activators enhances pro-thyrotrophin-releasing hormone (pro-TRH) transcription, co-incubation with both stimuli reduces this enhancement. In the present study, we used primary cultures of hypothalamic cells to test whether the order of these stimuli alters the cross-talk. We observed that a simultaneous or 1-h prior (but not later) activation of GR is necessary to inhibit the stimulatory effect of PKA activation on pro-TRH expression. We tested these in vitro results in the context of a physiological stimulus on the HPT axis in adult male rats. Cold exposure for 1 h enhanced pro-TRH mRNA expression in neurones of the hypophysiotrophic and rostral subdivisions of the paraventricular nucleus (PVN) of the hypothalamus, thyrotrophin (TSH) serum levels and deiodinase 2 (D2) activity in brown adipose tissue (BAT). An i.p. injection of corticosterone stimulated pro-TRH expression in the PVN of rats kept at ambient temperature, more pronouncedly in hypophysiotrophic neurones that no longer responded to cold exposure. In corticosterone-pretreated rats, the cold-induced increase in pro-TRH expression was detected only in the rostral PVN. Corticosterone blunted the increase in serum TSH levels and D2 activity in BAT produced by cold in vehicle-injected animals. Thus, increased serum corticosterone levels rapidly restrain cold stress-induced activation of TRH hypophysiotrophic neurones, which may contribute to changing energy expenditure. Interestingly, TRH neurones of the rostral PVN responded to both corticosterone and cold exposure with an amplified expression of pro-TRH mRNA, suggesting that these neurones integrate stress and temperature distinctly from the hypophysiotrophic neurones.