Floral thermal biology in relation to pollen thermal performance in an early spring flowering plant.

The floral microenvironment impacts gametophyte viability and plant-pollinator interactions. Plants employ mechanisms to modify floral temperature, including thermogenesis, absorption of solar radiation, and evaporative cooling. Whether floral thermoregulation impacts reproductive fitness, and how floral morphological variation mediates thermoregulatory capacity are poorly understood. We measured temperature of the floral microenvironment in the field and tested for thermogenesis in the lab in early spring flowering Hexastylis arifolia (Aristolochiaceae). We evaluated whether thermoregulatory capacity was associated with floral morphological variation. Finally, we experimentally determined the thermal optimum and tolerance of pollen to assess whether thermoregulation may ameliorate thermal stress to pollen. Pollen germination was optimal near 21 °C, with a 50% tolerance breadth of ~18 °C. In laboratory conditions, flowers exhibited thermogenesis of 1.5-4.8 °C for short intervals within a conserved timeframe (08:00-09:00 h). In the field, temperature inside the floral tube often deviated from ambient - floral interiors were up to 4 °C above ambient when it was cold, but some fell nearly 10 °C below ambient during peak heat. Flowers with smaller openings were cooler and more thermally stable than those with larger openings during peak heat. Thermoregulation maintained a floral microenvironment within the thermal tolerance breadth of pollen. Results suggest that H. arifolia flowers have a stronger capacity to cool than to warm, and that narrower floral openings create a distinct floral microenvironment, enhancing floral cooling effects. While deviation of floral temperature from ambient conditions maintains a suitable environment for pollen and suggests an adaptive role of thermoregulation, we discuss adaptive and nonadaptive mechanisms underlying floral warming and cooling.

Thunderstorm outflows preceding epidemics of asthma during spring and summer.

BACKGROUND: A study was undertaken to assess the importance of thunderstorms as a cause of epidemics of asthma exacerbations and to investigate the underlying mechanism. METHODS: A case control study was performed in six towns in south eastern Australia. Epidemic case days (n = 48) and a random sample of control days (n = 191) were identified by reference to the difference between the observed and expected number of emergency department attendances for asthma. The occurrence of thunderstorms, their associated outflows and cold fronts were ascertained, blind to case status, for each of these days. In addition, the relation of hourly pollen counts to automatic weather station data was examined in detail for the period around one severe epidemic of asthma exacerbations. The main outcome measure was the number of epidemics of asthma exacerbations. RESULTS: Thunderstorm outflows were detected on 33% of epidemic days and only 3% of control days (odds ratio 15.0, 95% confidence interval 6.0 to 37.6). The association was strongest in late spring and summer. Detailed examination of one severe epidemic showed that its onset coincided with the arrival of the thunderstorm outflow and a 4-12 fold increase in the ambient concentration of grass pollen grains. CONCLUSIONS: These findings are consistent with the hypothesis that some epidemics of exacerbations of asthma are caused by high concentrations of allergenic particles produced by an outflow of colder air, associated with the downdraught from a thunderstorm, sweeping up pollen grains and particles and then concentrating them in a shallow band of air at ground level. This is a common cause of exacerbations of asthma during the pollen season.