Impact of solid fuel usage on respiratory symptoms among reproductive aged women: a cross-sectional study in Sri Lanka.

BACKGROUND: Worldwide, around 3 billion people rely on solid fuel for their daily energy needs. Household air pollution secondary to solid fuel burning is a major risk factor for respiratory mobility among vulnerable populations. This study aimed to investigate the respiratory symptoms associated with solid fuel usage, the level of kitchen fuel smoke exposure and its association with respiratory symptoms among reproductive-aged women in Sri Lanka, where most households exclusively use firewood as the primary cooking fuel. METHODS: A descriptive cross-sectional study was conducted among 403 reproductive-aged women (15 to 49 years) in the Central Province, Sri Lanka. A structured interviewer-administered questionnaire was used to collect data, and an exposure assessment was done using a breath carbon monoxide monitor. RESULTS: After adjusting for potential confounding factors by the logistic regression models, the odds ratios (OR) of the liquid petroleum gas-only users for at least one respiratory symptom relevant to cough (OR: 0.39; 95% confidence interval [CI]: 0.20-0.78), wheezing (OR: 0.47; 95% [CI]: 0.26-0.87), and dyspnea (OR: 0.44; 95% CI: 0.24-0.84) were significantly lower compared to firewood-only users. The mean of expired air carbon monoxide and estimated carboxyhemoglobin levels of liquid petroleum gas-only users (2.84 ± 2.85 ppm; 1.08 ± 0.46%) were significantly lower than those of firewood-only users (5.27 ± 4.64 ppm; 1.47 ± 0.74%). CONCLUSIONS: The use of firewood increased the risk of respiratory symptoms among reproductive-aged women in Sri Lanka. Health education focused on positive behavioral changes and effective and efficient clean energy policies are recommended to mitigate the risk associated with solid fuel smoke exposure.

Clinically relevant concentration of pregabalin has no acute inhibitory effect on excitation of dorsal horn neurons under normal or neuropathic pain conditions: An intracellular calcium-imaging study in spinal cord slices from adult rats.

Pregabalin is thought to exert its therapeutic effect in neuropathic pain via binding to α2δ-1 subunits of voltage-gated calcium (Ca(2+)) channels. However, the exact analgesic mechanism after its binding to α2δ-1 subunits remains largely unknown. Whether a clinical concentration of pregabalin (≈10µM) can cause acute inhibition of dorsal horn neurons in the spinal cord is controversial. To address this issue, we undertook intracellular Ca(2+)-imaging studies using spinal cord slices with an intact attached L5 dorsal root, and examined if pregabalin acutely inhibits the primary afferent stimulation-evoked excitation of dorsal horn neurons in normal rats and in rats with streptozotocin-induced painful diabetic neuropathy. Under normal conditions, stimulation of a dorsal root evoked Ca(2+) signals predominantly in the superficial dorsal horn. Clinically relevant (10µM) and a very high concentration of pregabalin (100µM) did not affect the intensity or spread of dorsal root stimulation-evoked Ca(2+) signals, whereas an extremely high dose of pregabalin (300µM) slightly but significantly attenuated Ca(2+) signals in normal rats and in diabetic neuropathic (DN) rats. There was no difference between normal rats and DN rats with regard to the extent of signal attenuation at all concentrations tested. These results suggest that the activity of dorsal horn neurons in the spinal cord is not inhibited acutely by clinical doses of pregabalin under normal or DN conditions. It is very unlikely that an acute inhibitory action in the dorsal horn is the main analgesic mechanism of pregabalin in neuropathic pain states.

Male rats require testosterone to develop contralateral digastric muscle activity in response to noxious stimulation of the temporomandibular joint.

The influence of testosterone on the postnatal development of reflex electromyographic (EMG) jaw muscle activity evoked by injection of mustard oil (MO) into the temporomandibular joint region and the later recurrence of this EMG activity after intravenous injection of naloxone, was studied in male rats. MO-evoked EMG activity in the contralateral digastric muscle and naloxone-induced recurrence of this EMG activity were fully developed in intact, 8-week-old rats. Castration at 4 weeks of age inhibited the development of the contralateral MO-evoked EMG activity, but did not influence the naloxone-induced recurrence. Contralateral MO-evoked responses were observed in 8-week-old castrated rats if they received testosterone replacement therapy beginning at 4 weeks of age. These data suggest that testosterone is required for the development of a contralateral nociceptive reflex in the digastric muscle of male rats.

Intrathecal administration of 5-HT(3) receptor agonist modulates jaw muscle activity evoked by injection of mustard oil into the temporomandibular joint in the rat.

The effect of intrathecal administration of the 5-HT(3) receptor agonist 2-methyl-5-hydroxytryptamine (2m-5HT) on jaw muscle activity evoked by mustard oil (MO) injection into the temporomandibular joint of anesthetized rats was examined. One microgram or 100 microg of 2m-5HT significantly enhanced or suppressed jaw muscle responses, respectively. Pre-administration of tropisetron, a 5-HT(3) receptor antagonist, attenuated the effect of 2m-5HT. These results indicate that activation of 5-HT(3) receptors can modulate trigeminal nociceptive responses.