Prevalence of handheld laser device use, exposure and associated injury.

BACKGROUND: This study assessed the use of and exposure to handheld laser devices by Canadians and the potential associated health risks. DATA AND METHODS: The 2019 Canadian Community Health Survey collected data from 12,397 Canadians on the prevalence of handheld laser exposure or use, and associated eye or skin injuries. RESULTS: In 2019, an estimated 12.4% (95% CI: 11.4% to 13.4%) of Canadians reported using a handheld laser device or being exposed to its beam in the previous year, and those between the ages of 12 and 17 represented 30.5% (95% CI: 26.6% to 34.4%) of users. The highest laser device use or exposure was among those with a university education (13.8%; 95% CI: 11.8% to 15.8%), and a significant trend was found over income categories (p < 0.0001). The highest prevalence of exposure or use involved laser pointers (69.4%; 95% CI: 65.4% to 73.4%), followed by laser toys (38.5%; 95% CI: 34.6% to 42.5%), laser torches (8.2%; 95% CI: 6.1% to 10.4%) and-lastly-search-and-rescue lasers (0.8%E; 95% CI: 0.3% to 1.2%). Overall, 0.7%E (95% CI: 0.2% to 1.2%) of Canadians reported discomfort or injury in the past 12 months. One-quarter (27.9%; 95% CI: 23.8% to 31.9%) of users had a laser beam intentionally directed toward their eyes or skin. Most users did not buy the device (56.3%; 95% CI: 52.1% to 60.5%), while 40.5% (95% CI: 36.2% to 44.7%) purchased it at a Canadian retail store or online (3.8%E; 95% CI: 2.6% to 5.0%). DISCUSSION: The prevalence of handheld laser device use and beam exposure was 12.4% (95% CI: 11.4% to 13.4%), representing approximately 3.9 million Canadians. While the number of reported injuries was low, ongoing surveillance helps assess the effectiveness of current risk management approaches for laser products.

Prevalence of laser beam exposure and associated injuries.

BACKGROUND: An increasing number of consumer laser products are available to Canadians, many being purchased from online retailers. Of particular concern are high-powered, handheld laser devices. This study was conducted to assess the impact of this influx of laser products on the number of laser-associated injuries in Canada. DATA AND METHODS: The rapid response component of the 2014 Canadian Community Health Survey collected data from 19,765 Canadians on the prevalence of laser product exposure and usage, the type of laser product used, and the incidence of eye or skin injuries. RESULTS: Approximately half of Canadians (48.1%) reported using or being exposed to a laser product in the previous 12 months. The highest laser product usage or exposure was among those with university education (58.6%) and those with higher income categories (p ⟨ 0.0001). The highest prevalence of exposure or usage involved laser scanners (38.7%), laser pointers (11.1%) and lasers for entertainment (9.7%). Overall, about 1% of Canadians reported discomfort or injury involving a laser product in the past 12 months. Over half the injuries (59.1%) occurred to the eyes. Most of the injuries (74.9%) resulted from someone else's use of the device. The majority of the reported injuries were caused by lasers for cosmetic treatment or laser pointers. DISCUSSION: Despite the prevalence of laser product usage and exposure among Canadians, a low percentage of respondents reported injuries. This is likely because most laser devices are low-powered and typically do not represent a hazard. Nonetheless, efforts to increase awareness of laser product risks may be beneficial given the findings of this study.

Transcriptome analysis in mouse skin after exposure to ultraviolet radiation from a canopy sunbed.

Exposure to ultraviolet radiation (UV-R), from both natural and artificial tanning, heightens the risk of skin cancer by inducing molecular changes in cells and tissues. Despite established transcriptional alterations at a molecular level due to UV-R exposure, uncertainties persist regarding UV radiation characterization and subsequent genomic changes. Our study aimed to mechanistically explore dose- and time-dependent gene expression changes, that may drive short-term (e.g., sunburn) and long-term actinic (e.g., skin cancer) consequences. Using C57BL/6N mouse skin, we analyzed transcriptomic expression following exposure to five erythemally weighted UV-R doses (0, 5, 10, 20, and 40 mJ/cm2) emitted by a UV-R tanning device. At 96 h post-exposure, 5 mJ/cm2 induced 116 statistically significant differentially expressed genes (DEGs) associated with structural changes from UV-R damage. The highest number of significant gene expression changes occurred at 6 and 48 h post-exposure in the 20 and 40 mJ/cm2 dose groups. Notably, at 40 mJ/cm2, 13 DEGs related to skin barrier homeostasis were consistently perturbed across all timepoints. UV-R exposure activated pathways involving oxidative stress, P53 signaling, inflammation, biotransformation, skin barrier maintenance, and innate immunity. This in vivo study's transcriptional data offers mechanistic insights into both short-term and potential non-threshold-dependent long-term health effects of UV-R tanning.

Prevalence of tanning equipment use among Canadians.

The objective of this study was to collect prevalence estimates of indoor tanning usage and associated injuries in Canada. The rapid response component of the 2019 Canadian Community Health Survey collected data on the use of tanning equipment in the previous 12 months, including reasons for use, frequency/duration of use, precautions taken and adverse reactions or injuries. The 2019 research findings were as follows, an estimated 3.0% (95% CI: 2.5-3.4%) of Canadians reported that they had used indoor tanning equipment in the past year. Among users, 71.1% (95% CI: 63.9-78.3%) were female and females aged 18-34 were significantly more prevalent users compared to females aged 45 or older. The prevalence of indoor tanning was higher among people without a university degree; however, there were no differences in prevalence by household income or region. Most users indicated they used indoor tanning equipment within a tanning salon (75.3%: 95% CI: 69.1-81.6%) and the most common reason for usage was to develop a "protective" base tan (72.1%: 95% CI: 65.2-78.9%). Over one third (39.2%: 95% CI: 31.1-47.2%) of all users reported 10 or more sessions in the past year. The prevalence of indoor UV tanning usage is declining in Canada. Similar to results in 2014, the majority of users continue to be female, with a large number in the 18 to 34 age group.

Effects of 1800 MHz radiofrequency fields on signal transduction and antioxidant proteins in human A172 glioblastoma cells.

PURPOSE: To assess the effects of 1800 MHz radiofrequency electromagnetic field (RF-EMF) exposure on the expression of signal transduction and antioxidant proteins in a human-derived A172 glioblastoma cell line. MATERIALS AND METHODS: Adherent human-derived A172 glioblastoma cells (1.0 × 105 cells per 35 mm culture dish, containing 2 mL DMEM media) were exposed to 1800 MHz continuous-wave (CW) or GSM-modulated RF fields, in the presence or absence of serum for 5, 30 or 240 min at a specific absorption rate (SAR) of 0 (sham) or 2.0 W/kg. Concurrent negative (vehicle) and positive controls (1 µg/mL anisomycin) were included in each experiment. Cell lysates were collected immediately after exposure, stabilized by protease and phosphatase inhibitors in lysis buffer, then frozen and maintained at -80 °C until analysis. The relative expression levels of phosphorylated- and total-signal transduction proteins (CREB, JNK, NF-κB, ERK1/2, Akt, p70S6K, STAT3 and STAT5) and antioxidant proteins (SOD1, SOD2, CAT, TRX1, PRX2) were assessed using Milliplex magnetic bead array panels and a MagPix Multiplex imaging system. RESULTS: In cells exposed to 1800 MHz continuous-wave RF-EMF with the presence of serum in the culture medium, CAT expression was statistically significantly decreased after a 30 min exposure, total JNK was decreased at both 30 and 240 min of exposure, STAT3 was decreased after 240 min of exposure and phosphorylated-CREB expression was decreased after 30 min of exposure. In cells exposed to 1800 MHz GSM-modulated RF-EMF in serum-free cultures, the expression level of total STAT5 was decreased after 30 and 240 min of exposure. These observed changes were detected sporadically across time-points, culture conditions and RF-EMF exposure conditions indicating the likelihood of false positive events. When cells were treated with anisomycin for 15 min as a positive control, dramatic increases in the expression of phosphorylated signaling proteins were observed in both serum-starved and serum-fed A172 cells, with larger fold change increases in the serum-free cultures. No statistically significant differences in the expression levels of SOD1, SOD2 or TRX1 were observed under any tested conditions after exposure to RF-EMF. CONCLUSIONS: The current study found no consistent evidence of changes in the expression of antioxidant proteins (SOD1, SOD2, CAT or TRX2) or a variety of signal transductions proteins (CREB, JNK, NF-κB, ERK1/2, Akt, p70S6K, STAT3, STAT5) in a human-derived glioblastoma A172 cell line in response to exposure to 1800 MHz continuous-wave or GSM-modulated RF-EMF for 5, 30 or 240 min in either serum-free or serum-containing cultures.

Survey of reported eye injuries from handheld laser devices in Canada.

BACKGROUND: Unprotected exposure to handheld lasers can cause temporary or permanent vision loss depending on the laser classification. OBJECTIVE: To evaluate the occurrence of, and details associated with, reported eye injuries resulting from handheld lasers. METHODS: A 14-item questionnaire developed by Health Canada was distributed by the Canadian Ophthalmological Society and the Canadian Association of Optometrists to their respective members. RESULTS: Questionnaire data were available from 909 respondents (263 ophthalmologists; 646 optometrists). Response rates were 23.1% and 12.7%, respectively. Validated data were available from 903 respondents, where 157 (17.4%) reported encountering at least 1 eye injury from a handheld laser. A total of 318 eye injuries were reported with an annual increase of 34.4% (95% CI 21.6%-48.7%, p < 0.0001) between 2013 and 2017. When respondents reported on only their most severe case, 77 (53.5%) reported vision loss that ranged from minor to severe, which persisted for more than 6 months in 42.9% of the cases. Another 59 (41.3%) noted the presence of retinal damage. The prevalence of eye injuries from handheld lasers was higher for males (82.5%) than females (14.0%), more frequent among those under the age of 50 years, and occurred predominately as a result of exposure from another person (67.6%) versus self-induced (26.1%) (p < 0.0001). CONCLUSIONS: Although this pilot study permits insight into the potential prevalence of injuries resulting from exposure to handheld laser devices in Canada, the results are not nationally representative. These findings support additional surveillance activities that may inform risk assessment and potential risk management strategies.

The application of transcriptional benchmark dose modeling for deriving thresholds of effects associated with solar-simulated ultraviolet radiation exposure.

Considerable data has been generated to elucidate the transcriptional response of cells to ultraviolet radiation (UVR) exposure providing a mechanistic understanding of UVR-induced cellular responses. However, using these data to support standards development has been challenging. In this study, we apply benchmark dose (BMD) modeling of transcriptional data to derive thresholds of gene responsiveness following exposure to solar-simulated UVR. Human epidermal keratinocytes were exposed to three doses (10, 20, 150 kJ/m2 ) of solar simulated UVR and assessed for gene expression changes 6 and 24 hr postexposure. The dose-response curves for genes with p-fit values (≥ 0.1) were used to derive BMD values for genes and pathways. Gene BMDs were bi-modally distributed, with a peak at ∼16 kJ/m2 and ∼108 kJ/m2 UVR exposure. Genes/pathways within Mode 1 were involved in cell signaling and DNA damage response, while genes/pathways in the higher Mode 2 were associated with immune response and cancer development. The median value of each Mode coincides with the current human exposure limits for UVR and for the minimal erythemal dose, respectively. Such concordance implies that the use of transcriptional BMD data may represent a promising new approach for deriving thresholds of actinic effects. Environ. Mol. Mutagen. 59:502-515, 2018. © 2018 The Authors Environmental and Molecular Mutagenesis published by Wiley Periodicals, Inc. on behalf of Environmental Mutagen Society.

Transcriptomic profiling of radiation-resistant or -sensitive human colorectal cancer cells: acute effects of a single X-radiation dose.

We previously isolated several clones that were closely-related genetically from a human colorectal tumor (HCT116) cell line. These clones displayed significantly different X-radiation response phenotypes. In this paper, we investigated how a single dose of X-radiation modulated the transcriptomic profiles of either the radiation-resistant (HCT116Clone2_XRR) or the radiation-sensitive (HCT116CloneK_XRS) clone when each was compared to a reference clone, HCT116Clone10_control. The latter represented a control clone that displayed a similar X-radiation response as the parental HCT116 cells. Pooled RNAs were obtained from HCT116Clone2_XRR, HCT116CloneK_XRS or HCT116Clone10_control cells either before or at 10 min, 6 or 24 h after treatment with 4-Gy X-radiation. Transcriptomic profiles were assessed by cDNA microarrays. At least three independent experiments were carried out for each time point and statistical analysis was performed by paired t-test (p<0.05). From 19,200 genes/ESTs examined, we identified only 120 genes/ESTs that were differentially expressed at any one of these four time points. Interestingly, different patterns of gene modulation were observed between the radiation-sensitive and radiation-resistant clones. However, the fold changes of gene modulation were generally small (2-3 fold). Surprisingly, only 12.7% of 79 genes involved in DNA damage sensor/repair and cell cycle and between 2.6 and 9.2% of 76 genes involved in apoptosis, were significantly modulated in these early time points following irradiation. By comparison, up to 10% of 40 known housekeeping genes were differentially expressed. Thus in our experimental model, we were able to detect the up-regulation or down-regulation of mostly novel genes and/or pathways in the acute period (up to 24 h) following a single dose of 4-Gy X-radiation.

Fractionated X-radiation treatment can elicit an inducible-like radioprotective response that is not dependent on the intrinsic cellular X-radiation resistance/sensitivity.

Inducible responses are well documented to play a role in the radiation response of cells. However, it is not known whether clinically relevant fractionated X-radiation treatment could elicit an inducible-like radioprotective response and whether there is a direct correlation between the inducible radiation response phenomenon and the intrinsic radiation response of the cell. Therefore, the purpose of this study was to determine whether closely related human colorectal tumor (HCT116) clones treated with fractionated X rays could elicit an inducible-like radiation response to a subsequent acute (i.e. single) X-ray challenge, and whether the magnitude of the inducible-like response correlates with the intrinsic X-ray resistance of the responding clones. After fractionated X irradiation, only the radiosensitive clone showed enhanced clonogenic survival with a subsequent acute X-ray exposure. Cell cycle changes or the selection of subclones with increased intrinsic radiation resistance induced by the fractionated X rays were excluded as the basis of this enhanced tolerance, suggesting the presence of an inducible-like radioprotective response. Using the comet assay, we found similar amounts of intrinsic DNA damage among the clones after acute X irradiation. Our findings demonstrate that fractionated X-ray treatment can elicit an inducible-like radioprotective response and represent the first evidence that this response is independent of the intrinsic radiation resistance/sensitivity of the responding cells.

Effects of N1, N13-diethylnorspermine (DENSPM) and X-radiation treatment on human colorectal tumor clones with varying X-radiation and drug responses.

This study was designed to examine the effects of treatment with N1, N13-diethylnorspermine (DENSPM), a spermine analog, and X radiation on survival and on the polyamine and spermidine/spermine N1-acetyltransferase (SSAT) levels in closely related human colorectal tumor (HCT116) clones exhibiting a wide range of X-radiation and drug responses. After treatment with DENSPM and X radiation, clonogenic cell survival was measured. SSAT protein levels were measured by Western blot analysis and SSAT enzymatic activities by the conversion of [1-14C]acetyl-CoA into [1-14C]acetylspermidine. Polyamine [i.e. putrescine (PUT), spermine (SPM) and spermidine (SPD)] levels were measured with high-performance liquid chromatography. DENSPM enhanced the efficacy of radiation treatment in HCT116, HCT116-Clone2 (a radiation-resistant clone) and HCT116-Clone10 (a clone with similar X-radiation response as the parental HCT116 cells) but not in HCT116-CloneK (an X-radiation-sensitive but relatively drug-resistant clone). Treatment with DENSPM without X radiation caused the most significant increase in SSAT activity (approximately 22-fold) and an almost complete depletion of SPD levels in HCT116-CloneK. Our results suggest that (a) the lack of sensitization of X-radiation treatment by DENSPM in HCT116-CloneK was likely due to the prior depletion of SPD levels by DENSPM alone, (b) natural polyamine contents and/or inducibility of SSAT may be important factors influencing cellular response to combined X-radiation and DENSPM treatments, and (c) more importantly, there may be a potentially novel role for combining polyamine analogs such as DENSPM with X rays.

Comparison of the X-radiation, drug and ultraviolet-radiation responses of clones isolated from a human colorectal tumor cell line.

We isolated several clones with a wide range of responses to X radiation from an unirradiated human colorectal (HCT 116) tumor cell line. The responses of one of these clones (HCT116-Clone10) and nine other clones to either fractionated or acute (i.e. single, nonfractionated doses) X irradiation in vitro was similar to that of the parental cell line. By contrast, after the same types of treatment, another clone (HCT116-Clone2) manifested a significantly increased survival whereas a third clone (HCT116-CloneK) manifested a significantly decreased survival relative to the parental cell line. This suggested that they were, respectively, a radioresistant and a radiosensitive clone. All three clones (clones 2, 10, K) retained their tumorigenic phenotype and formed tumors in nude mice. G-banding studies demonstrated that they were of human origin and were derived from the same parental cell line. The metaphases of HCT116-Clone2 demonstrated features commonly associated with genomic instability (i.e. mitotic catastrophe including chromosome and chromatid breaks, dicentrics and additional nonclonal markers). Data obtained by quantitative fluorescence in situ hybridization (Q- FISH) analysis failed to demonstrate any apparent correlation between the radiosensitivity and the relative telomere content of these three clones. Interestingly, HCT116-CloneK was the most resistant to several chemotherapeutic drugs (topotecan, camptothecin, etoposide and cisplatin) with diverse mechanisms of action. Also, there were no significant differences in the survivals of the three clones after treatment with UV radiation. Because of the lack of overlap among the relative sensitivities of these clones to X radiation, chemotherapeutic drugs and UV radiation, these clones may be useful models for evaluating the genetic basis of the response of human tumor cells to these treatment agents both in vitro and in vivo.

Analysis of gene expression in two human-derived cell lines exposed in vitro to a 1.9 GHz pulse-modulated radiofrequency field.

There is considerable controversy surrounding the biological effects of radiofrequency (RF) fields, as emitted by mobile phones. Previous work from our laboratory has shown no effect related to the exposure of 1.9 GHz pulse-modulated RF fields on the expression of 22,000 genes in a human glioblastoma-derived cell-line (U87MG) at 6 h following a 4 h RF field exposure period. As a follow-up to this study, we have now examined the effect of RF field exposure on the possible expression of late onset genes in U87MG cells after a 24 h RF exposure period. In addition, a human monocyte-derived cell-line (Mono-Mac-6, MM6) was exposed to intermittent (5 min ON, 10 min OFF) RF fields for 6 h and then gene expression was assessed immediately after exposure and at 18 h postexposure. Both cell lines were exposed to 1.9 GHz pulse-modulated RF fields for 6 or 24 h at specific absorption rates (SARs) of 0.1-10.0 W/kg. In support of our previous results, we found no evidence that nonthermal RF field exposure could alter gene expression in either cultured U87MG or MM6 cells, relative to nonirradiated control groups. However, exposure of both cell-lines to heat-shock conditions (43 degrees C for 1 h) caused an alteration in the expression of a number of well-characterized heat-shock proteins.