Shlezinger M, Amitai Y, Goldenberg I, Shechter M. Desalinated seawater supply and all-cause mortality in hospitalized acute myocardial infarction patients from the Acute Coronary Syndrome Israeli Survey 2002-2013. International Journal of Cardiology. 2016 Jun 29;220:544-550. doi: 10.1016/j.ijcard.2016.06.241.
BACKGROUND: Consuming desalinated seawater (DSW) as drinking water (DW) may reduce magnesium in water intake causing hypomagnesemia and adverse cardiovascular effects.
METHODS: We evaluated 30-day and 1-year all-cause mortality of acute myocardial infarction (AMI) patients enrolled in the biannual Acute Coronary Syndrome Israeli Survey (ACSIS) during 2002-2013. Patients (n=4678) were divided into 2 groups: those living in regions supplied by DSW (n=1600, 34.2%) and non-DSW (n=3078, 65.8%). Data were compared between an early period [2002-2006 surveys (n=2531) – before desalination] and a late period [2008-2013 surveys (n=2147) – during desalination].
RESULTS: Thirty-day all-cause-mortality was significantly higher in the late period in patients from the DSW regions compared with those from the non-DSW regions (HR=2.35 CI 95% 1.33-4.15, P<0.001) while in the early period there was no significant difference (HR=1.37 CI 95% 0.9-2, P=0.14). Likewise, there was a significantly higher 1-year all-cause mortality in the late period in patients from DSW regions compared with those from the non-DSW regions (HR=1.87 CI 95% 1.32-2.63, P<0.0001), while in the early period there was no significant difference (HR=1.17 CI 95% 0.9-1.5, P=0.22). Admission serum magnesium level (M±SD) in the DSW regions (n=130) was 1.94±0.24mg/dL compared with 2.08±0.27 mg/dL in 81 patients in the non-DSW (P<0.0001).
CONCLUSIONS: Higher 30-day and 1-year all-cause mortality in AMI patients, found in the DSW regions may be attributed to reduced magnesium intake secondary to DSW consumption.
This sort of charade gets us nowhere when it comes to addressing the real issues associated with changes in climate. These senators will only succeed in creating more ill-will.
“Democratic senators have been assigned conservative nonprofit groups to call out by name on the chamber floor in speeches on Monday and Tuesday criticizing corporations and advocacy groups for opposing Democratic climate policies, internal emails reveal.
Nineteen Senate Democrats will attack specific organizations in what they are calling a “web of denial,” according to a schedule of floor speeches circulated by Emily Enderle, a top environmental policy adviser to Sen. Sheldon Whitehouse (D., R.I.), who is spearheading the effort.” click here
Wei R, Luo G, Sun Z, Wang S, Wang J. Chronic fluoride exposure-induced testicular toxicity is associated with inflammatory response in mice. Chemosphere 2016 Jun;153:419-25. doi: 10.1016/j.chemosphere.2016.03.045.
Previous studies have indicated that fluoride (F) can affect testicular toxicity in humans and rodents. However, the mechanism underlying F-induced testicular toxicity is not well understood. This study was conducted to evaluate the sperm quality, testicular histomorphology and inflammatory response in mice followed F exposure. Healthy male mice were randomly divided into four groups with sodium fluoride (NaF) at 0, 25, 50, 100 mg/L in the drinking water for 180 days. At the end of the exposure, significantly increased percentage of spermatozoa abnormality was found in mice exposed to 50 and 100 mg/L NaF. Disorganized spermatogenic cells, vacuoles in seminiferous tubules and loss and shedding of sperm cells were also observed in the NaF treated group. In addition, chronic F exposure increased testicular interleukin-17(IL-17), interleukin-17 receptor C (IL-17RC), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in transcriptional levels, as well as IL-17 and TNF-α levels in translational levels. Interestingly, we observed that F treated group elevated testicular inducible nitric oxide synthase (iNOS) mRNA level and nitric oxide (NO) concentration. Taken together, these results indicated that testicular inflammatory response could contribute to chronic F exposure induced testicular toxicity in mice.