Hydrogen sulfide (H2S) is a toxic gas that is well-known for its acute health risks in occupational settings, but less is known about effects of chronic and low-level exposures. This critical review investigates toxicological and experimental studies, exposure sources, standards, and epidemiological studies pertaining to chronic exposure to H2S from both natural and anthropogenic sources. H2S releases, while poorly documented, appear to have increased in recent years from oil and gas and possibly other facilities. Chronic exposures below 10 ppm have long been associated with odor aversion, ocular, nasal, respiratory and neurological effects. However, exposure to much lower levels, below 0.03 ppm (30 ppb), has been associated with increased prevalence of neurological effects, and increments below 0.001 ppm (1 ppb) in H2S concentrations have been associated with ocular, nasal, and respiratory effects. Many of the studies in the epidemiological literature are limited by exposure measurement error, co-pollutant exposures and potential confounding, small sample size, and concerns of representativeness, and studies have yet to consider vulnerable populations. Long-term community-based studies are needed to confirm the low concentration findings and to refine exposure guidelines. Revised guidelines that incorporate both short- and long-term limits are needed to protect communities, especially sensitive populations living near H2S sources.

Preeclampsia is becoming an increasingly common diagnosis in the developed world and remains a high cause of maternal and fetal morbidity and mortality in the developing world. Delay in childbearing in the developed world feeds into the risk factors associated with preeclampsia, which include older maternal age, obesity, and/or vascular diseases. Inadequate prenatal care partially explains the persistent high prevalence in the developing world. In this review, we begin by presenting the most recent concepts in the pathogenesis of preeclampsia. Upstream triggers of the well described angiogenic pathways, such as the heme oxygenase and hydrogen sulfide pathways, as well as the roles of autoantibodies, misfolded proteins, nitric oxide, and oxidative stress will be described. We also detail updated definitions, classification schema, and treatment targets of hypertensive disorders of pregnancy put forth by obstetric and hypertensive societies throughout the world. The shift has been made to view preeclampsia as a systemic disease with widespread endothelial damage and the potential to affect future cardiovascular diseases rather than a self-limited occurrence. At the very least, we now know that preeclampsia does not end with delivery of the placenta. We conclude by summarizing the latest strategies for prevention and treatment of preeclampsia. A better understanding of this entity will help in the care of at-risk women before delivery and for decades after.

The effect of decreasing the number of animals on the accuracy of estimated concentration-time-mortality relationships and the LC50 values derived from these was investigated by means of simulation methods. Studies of NH3, Cl2, H2S, and COCl2 were made using 5 rats per sex per group. Mortality rates were analysed in 500 new data sets obtained by randomly removing 4 rats/sex/group from the original data sets. It was concluded that the concentration-time-mortality relationship and the LC50 values can be determined over a 5-10-fold time range using one rat/sex/group. The resulting 5 and 95 percentiles compare favourably with the 90% confidence limits when determining a LC50 according to OECD guideline 403. When using concentration-time-mortality relationships, additional information can be obtained which can be used in inhalation hazard risk assessment.