Tanning bed use and melanoma: Establishing risk and improving prevention interventions

AbstractPurposeExposure to ultraviolet radiation (UVR) from indoor tanning devices is thought to cause melanoma and other negative health consequences. Despite these findings, the practice of indoor tanning in the United States remains prevalent. In this paper we aim to present a clear discussion of the relationship between indoor tanning and melanoma risk, and to identify potential strategies for effective melanoma prevention by addressing indoor tanning device use.Basic proceduresWe reviewed relevant literature on the risks of indoor tanning, current indoor tanning legislation, and trends in indoor tanning and melanoma incidence. Study was conducted at the University of Southern California, Los Angeles, CA between the years of 2014 and 2015.Main findingsOur findings reaffirm the relationship between indoor tanning and melanoma risk, and suggest a widespread public misunderstanding of the negative effects of indoor tanning.Principal conclusionsThis review argues for an aggressive initiative to reduce indoor tanning in the United States, to design prevention efforts tailored towards specific high risk groups, and the need to better inform the public of the risks of indoor tanning

An effective and efficient approach for manually improving geocoded data

<p>Abstract</p> <p>Background</p> <p>The process of geocoding produces output coordinates of varying degrees of quality. Previous studies have revealed that simply excluding records with low-quality geocodes from analysis can introduce significant bias, but depending on the number and severity of the inaccuracies, their inclusion may also lead to bias. Little quantitative research has been presented on the cost and/or effectiveness of correcting geocodes through manual interactive processes, so the most cost effective methods for improving geocoded data are unclear. The present work investigates the time and effort required to correct geocodes contained in five health-related datasets that represent examples of data commonly used in Health GIS.</p> <p>Results</p> <p>Geocode correction was attempted on five health-related datasets containing a total of 22,317 records. The complete processing of these data took 11.4 weeks (427 hours), averaging 69 seconds of processing time per record. Overall, the geocodes associated with 12,280 (55%) of records were successfully improved, taking 95 seconds of processing time per corrected record on average across all five datasets. Geocode correction improved the overall match rate (the number of successful matches out of the total attempted) from 79.3 to 95%. The spatial shift between the location of original successfully matched geocodes and their corrected improved counterparts averaged 9.9 km per corrected record. After geocode correction the number of city and USPS ZIP code accuracy geocodes were reduced from 10,959 and 1,031 to 6,284 and 200, respectively, while the number of building centroid accuracy geocodes increased from 0 to 2,261.</p> <p>Conclusion</p> <p>The results indicate that manual geocode correction using a web-based interactive approach is a feasible and cost effective method for improving the quality of geocoded data. The level of effort required varies depending on the type of data geocoded. These results can be used to choose between data improvement options (e.g., manual intervention, pseudocoding/geo-imputation, field GPS readings).</p

Solar ultraviolet radiation exposure, and incidence of childhood acute lymphocytic leukaemia and non-Hodgkin lymphoma in a US population-based dataset

Background: Acute lymphocytic leukaemia (ALL) and non-Hodgkin lymphoma (NHL) are among the commonest types of childhood cancer. Some previous studies suggested that elevated ultraviolet radiation (UVR) exposures increase ALL risk; many more indicate NHL risk is reduced. Methods: We assessed age&lt;20 ALL/NHL incidence in Surveillance, Epidemiology and End Results data using AVGLO-derived UVR irradiance/cumulative radiant exposure measures, using quasi-likelihood models accounting for underdispersion, adjusted for age, sex, racial/ethnic group and other county-level socioeconomic variables. Results: There were 30,349 cases of ALL and 8062 of NHL, with significant increasing trends of ALL with UVR irradiance (relative risk (RR) = 1.200/mW/cm2 (95% CI 1.060, 1.359, p = 0.0040)), but significant decreasing trends for NHL (RR = 0.646/mW/cm2 (95% CI 0.512, 0.816, p = 0.0002)). There was a borderline-significant increasing trend of ALL with UVR cumulative radiant exposure (RR = 1.444/MJ/cm2 (95% CI 0.949, 2.197, p = 0.0865)), and significant decreasing trends for NHL (RR = 0.284/MJ/cm2 (95% CI 0.166, 0.485, p &lt; 0.0001)). ALL and NHL trend RR is substantially increased among those aged 0–3. All-age trend RRs are most extreme (increasing for ALL, decreasing for NHL) for Hispanics for both UVR measures. Conclusions:Our more novel finding, of excess UVR-related ALL risk, is consistent with some previous studies, but is not clear-cut, and in need of replication.</p

Solar ultraviolet radiation exposure, and incidence of childhood acute lymphocytic leukaemia and non-Hodgkin lymphoma in a US population-based dataset

Background: Acute lymphocytic leukaemia (ALL) and non-Hodgkin lymphoma (NHL) are among the commonest types of childhood cancer. Some previous studies suggested that elevated ultraviolet radiation (UVR) exposures increase ALL risk; many more indicate NHL risk is reduced. Methods: We assessed age<20 ALL/NHL incidence in Surveillance, Epidemiology and End Results data using AVGLO-derived UVR irradiance/cumulative radiant exposure measures, using quasi-likelihood models accounting for underdispersion, adjusted for age, sex, racial/ethnic group and other county-level socioeconomic variables. Results: There were 30,349 cases of ALL and 8062 of NHL, with significant increasing trends of ALL with UVR irradiance (relative risk (RR) = 1.200/mW/cm2 (95% CI 1.060, 1.359, p = 0.0040)), but significant decreasing trends for NHL (RR = 0.646/mW/cm2 (95% CI 0.512, 0.816, p = 0.0002)). There was a borderline-significant increasing trend of ALL with UVR cumulative radiant exposure (RR = 1.444/MJ/cm2 (95% CI 0.949, 2.197, p = 0.0865)), and significant decreasing trends for NHL (RR = 0.284/MJ/cm2 (95% CI 0.166, 0.485, p  Conclusions: Our more novel finding, of excess UVR-related ALL risk, is consistent with some previous studies, but is not clear-cut, and in need of replication

Aldehyde dehydrogenase inhibition as a pathogenic mechanism in Parkinson disease

Parkinson disease (PD) is a neurodegenerative disorder particularly characterized by the loss of dopaminergic neurons in the substantia nigra. Pesticide exposure has been associated with PD occurrence, and we previously reported that the fungicide benomyl interferes with several cellular processes potentially relevant to PD pathogenesis. Here we propose that benomyl, via its bioactivated thiocarbamate sulfoxide metabolite, inhibits aldehyde dehydrogenase (ALDH), leading to accumulation of the reactive dopamine metabolite 3,4-dihydroxyphenylacetaldehyde (DOPAL), preferential degeneration of dopaminergic neurons, and development of PD. This hypothesis is supported by multiple lines of evidence. (i) We previously showed in mice the metabolism of benomyl to S-methyl N-butylthiocarbamate sulfoxide, which inhibits ALDH at nanomolar levels. We report here that benomyl exposure in primary mesencephalic neurons (ii) inhibits ALDH and (iii) alters dopamine homeostasis. It induces selective dopaminergic neuronal damage (iv) in vitro in primary mesencephalic cultures and (v) in vivo in a zebrafish system. (vi) In vitro cell loss was attenuated by reducing DOPAL formation. (vii) In our epidemiology study, higher exposure to benomyl was associated with increased PD risk. This ALDH model for PD etiology may help explain the selective vulnerability of dopaminergic neurons in PD and provide a potential mechanism through which environmental toxicants contribute to PD pathogenesis

Socioeconomic status and prostate cancer incidence and mortality rates among the diverse population of California

The racial/ethnic disparities in prostate cancer rates are well documented, with the highest incidence and mortality rates observed among African-Americans followed by non-Hispanic Whites, Hispanics, and Asian/Pacific Islanders. Whether socioeconomic status (SES) can account for these differences in risk has been investigated in previous studies, but with conflicting results. Furthermore, previous studies have focused primarily on the differences between African-Americans and non-Hispanic Whites, and little is known for Hispanics and Asian/Pacific Islanders. To further investigate the relationship between SES and prostate cancer among African-Americans, non-Hispanic Whites, Hispanics, and Asian/Pacific Islanders, we conducted a large population-based cross-sectional study of 98,484 incident prostate cancer cases and 8,997 prostate cancer deaths from California. Data were abstracted from the California Cancer Registry, a population-based surveillance, epidemiology, and end results (SEER) registry. Each prostate cancer case and death was assigned a multidimensional neighborhood-SES index using the 2000 US Census data. SES quintile-specific prostate cancer incidence and mortality rates and rate ratios were estimated using SEER*Stat for each race/ethnicity categorized into 10-year age groups. For prostate cancer incidence, we observed higher levels of SES to be significantly associated with increased risk of disease [SES Q1 vs. Q5: relative risk (RR) = 1.28; 95% confidence interval (CI): 1.25–1.30]. Among younger men (45–64 years), African-Americans had the highest incidence rates followed by non-Hispanic Whites, Hispanics, and Asian/Pacific Islanders for all SES levels. Yet, among older men (75–84 years) Hispanics, following African-Americans, displayed the second highest incidence rates of prostate cancer. For prostate cancer deaths, higher levels of SES were associated with lower mortality rates of prostate cancer deaths (SES Q1 vs. Q5: RR = 0.88; 95% CI: 0.92–0.94). African-Americans had a twofold to fivefold increased risk of prostate cancer deaths in comparison to non-Hispanic Whites across all levels of SES. Our findings suggest that SES alone cannot account for the greater burden of prostate cancer among African-American men. In addition, incidence and mortality rates of prostate cancer display different age and racial/ethnic patterns across gradients of SES

Current Data on Risk Factor Estimates Does Not Explain the Difference in Rates of Melanoma between Hispanics and Non-Hispanic Whites

United States Hispanics have seven times lower melanoma incidence rates than non-Hispanic whites (NHW). It is unclear whether this difference can be explained solely by phenotypic risk factors, like darker skin, or whether modifiable risk factors, like sun exposure, also play a role. The purpose of this paper is to summarize what is currently known about melanoma risk factors among Hispanics and NHWs, and whether or not those differences could explain the difference in melanoma incidence. Through literature review, relative risks and prevalence of melanoma risk factors in Hispanics and NHWs were identified and used to calculate the expected rate in Hispanics and rate ratio compared to NHWs. We found that melanoma risk factors either have similar frequency in Hispanics and NHWs (e.g., many large nevi) or are less frequent in Hispanics but do not explain a high proportion of disease variation (e.g., red hair). Considering current knowledge of risk factor prevalence, we found that melanoma incidence rates in the two groups should actually be similar. Sun exposure behavior among Hispanics may contribute to the explanation for the 7-fold difference in melanoma rates. Currently, limited data exist on sun exposure behavior among Hispanics, but possibilities for improving primary prevention by further studying these practices are substantial

Aldehyde dehydrogenase variation enhances effect of pesticides associated with Parkinson disease.

ObjectiveThe objective of this study was to determine whether environmental and genetic alterations of neuronal aldehyde dehydrogenase (ALDH) enzymes were associated with increased Parkinson disease (PD) risk in an epidemiologic study.MethodsA novel ex vivo assay was developed to identify pesticides that can inhibit neuronal ALDH activity. These were investigated for PD associations in a population-based case-control study, the Parkinson's Environment &amp; Genes (PEG) Study. Common variants in the mitochondrial ALDH2 gene were genotyped to assess effect measure modification (statistical interaction) of the pesticide effects by genetic variation.ResultsAll of the metal-coordinating dithiocarbamates tested (e.g., maneb, ziram), 2 imidazoles (benomyl, triflumizole), 2 dicarboxymides (captan, folpet), and 1 organochlorine (dieldrin) inhibited ALDH activity, potentially via metabolic byproducts (e.g., carbon disulfide, thiophosgene). Fifteen screened pesticides did not inhibit ALDH. Exposures to ALDH-inhibiting pesticides were associated with 2- to 6-fold increases in PD risk; genetic variation in ALDH2 exacerbated PD risk in subjects exposed to ALDH-inhibiting pesticides.ConclusionALDH inhibition appears to be an important mechanism through which environmental toxicants contribute to PD pathogenesis, especially in genetically vulnerable individuals, suggesting several potential interventions to reduce PD occurrence or slow or reverse its progression