Biomedical subjects

R D Saunders

Publications and source records attributed to R D Saunders.

75 records · Page 5Linked to original sources

PubMedDate not supplied

Dominant lethal studies in male mice after exposure to 2.45 GHz microwave radiation.

Adult male mice had the lower halves of their bodies exposed in a waveguide system to 2.45 GHz microwave radiation for 30 min. The half body dose-rate of 43 W kg-1 had been shown in a previous study [7] to deplete severely the heat-sensitive stages of sperm production. The males were mated at intervals to adult hybrid females over the following 8-10 weeks. There was no significant reduction in post-implantation survival, suggesting that the microwave exposure did not have a mutagenic effect on the male germ cells. However, pregnancy rate was significantly reduced in weeks 3, 4, 5 and 6; reaching a minimum of about 10% of the control value in weeks 4 and 5. The occurrence of low values in weeks 4 and 5 correlated well with the expected reductions in sperm count due to the pattern of depletion of the spermatogenic epithelium of the testes. Thus it was concluded that the reduced pregnancy rate resulted from reduced male fertility. Pre-implantation survival can also be affected by reduced sperm count [8] and was significantly reduced in this study but it correlated less well with the anticipated heat response. A further study is in progress looking at the contribution of sperm count and sperm abnormality to the results.

Animals↗

PubMedDate not supplied

Effects of heat on embryos and foetuses.

OBJECTIVES: This paper reviews the effects of elevated maternal temperature on embryo and foetal development in experimental animals and in humans. CONCLUSIONS: Hyperthermia during pregnancy can cause embryonic death, abortion, growth retardation and developmental defects. Processes critical to embryonic development, such as cell proliferation, migration, differentiation and programmed cell death (apoptosis) are adversely affected by elevated maternal temperatures, showing some similarity to the effects of ionizing radiation. The development of the central nervous system is especially susceptible: a 2.5 degrees C elevation for 1 h during early neural tube closure in rats resulted in an increased incidence of cranio-facial defects, and a 'spike' temperature elevation of 2-2.5 degrees C in an exposure of 1 h during early neurogenesis in guinea pigs caused an increase in the incidence of microencephaly. However, in general, thresholds and dose-response relationships vary between species and even between different strains of the same species, depending on genotype. This precludes rigorous quantitative extrapolation to humans, although some general principles can be inferred. In humans, epidemiological studies suggest that an elevation of maternal body temperature by 2 degrees C for at least 24 h during fever can cause a range of developmental defects, but there is little information on thresholds for shorter exposures. Further experimental and epidemiological studies are recommended, focusing on stage-specific developmental effects in the central nervous system using a variety of sensitive assays.

Animals↗

PubMedDate not supplied

Cardiovascular responses to heat stress and their adverse consequences in healthy and vulnerable human populations.

This paper reviews the basic thermoregulatory physiology of healthy people in relation to hazards from external heat stress and internal heat loads generated by physical exercise or radiofrequency (RF) radiation. In addition, members of the population are identified who may be particularly vulnerable to the effects of heat stress. These data are examined in relation to current international guidance on occupational and public exposure to RF radiation. When body temperature rises, heat balance of the body is normally restored by increased blood flow to the skin and by sweating. These responses increase the work of the heart and cause loss of salt and water from the body. They impair working efficiency and can overload the heart and cause haemoconcentration, which can lead to coronary and cerebral thrombosis, particularly in elderly people with atheromatous arteries. These adverse effects of thermoregulatory adjustments occur with even mild heat loads and account for the great majority of heat-related illness and death. They are, therefore, particularly relevant to determination of safe population exposures to additional sources of heat stress. It is concluded that exposure to RF levels currently recommended as safe for the general population, equivalent to heat loads of about one tenth basal metabolic rate, could continue to be regarded as trivial in this context, but that prolonged exposures of the general population to RF levels higher than that could not be regarded as safe in all circumstances.

Adaptation, Physiological↗